The theory of constructed emotion: an active inference
account of interoception and categorization
Lisa Feldman Barrett1,2,3
1
Department of Psychology, Northeastern University, Boston, MA, USA, 2
Athinoula, A. Martinos Center for
Biomedical Imaging and 3
Psychiatric Neuroimaging Division, Department of Psychiatry, Massachusetts
General Hospital and Harvard Medical School, Charlestown, MA, USA.
Correspondence should be addressed to Lisa Feldman Barrett. Department of Psychology, Northeastern University, Boston, MA, USA. E-mail: l.barrett@neu.edu
Abstract
The science of emotion has been using folk psychology categories derived from philosophy to search for the brain basis of
emotion. The last two decades of neuroscience research have brought us to the brink of a paradigm shift in understanding
the workings of the brain, however, setting the stage to revolutionize our understanding of what emotions are and how
they work. In this article, we begin with the structure and function of the brain, and from there deduce what the biological
basis of emotions might be. The answer is a brain-based, computational account called the theory of constructed emotion.
Key words: emotion; predictive coding; construction; interoception; categorization; concepts; affect
Ancient philosophers and physicians believed a human mind to
be a collection of mental faculties. They divided the mind, not
with an understanding of biology or the brain, but to capture
the essence of human nature according to their concerns about
truth, beauty and ethics. The faculties in question have
morphed over the millennia, but generally speaking, they
encompass mental categories for thinking (cognitions), feeling
(emotions) and volition (actions, and in more modern versions,
perceptions). These mental categories symbolize a cherished
narrative about human nature in Western civilization: that
emotions (our inner beast) and cognitions (evolution’s crowning
achievement) battle or cooperate to control behavior.1
The classical
view of emotion (Figure 1) was forged in these ancient
ideas. Affective neuroscience takes its inspiration from this
faculty-based approach. Scientists begin with emotion concepts
that are most recognizably English (Pavlenko, 2014; Wierzbicka,
2014), such as anger, sadness, fear, and disgust, and search for
their elusive biological essences (i.e. their neural signatures or
fingerprints), usually in subcortical regions. This inductive approach
assumes that the emotion categories we experience and
perceive as distinct must also be distinct in nature.
If the history of science has taught us anything, however, it
is that human experiences rarely reveal the way that the natural
world works: ‘Physical concepts are free creations of the
human mind, and are not; however, it may seem, uniquely
determined by the external world’ (Einstein et al., 1938, p. 33).
The last two decades of neuroscience research have brought us
to the brink of a paradigm shift in understanding the workings
of the brain, setting the stage to revolutionize our study of emotions
(or any mental category). So in this article, we turn the
typical inductive approach on its head. We begin not with mental
categories but with the structure and function of the brain,
and from there deduce what the biological basis of emotions
might be. The answer, I suggest, will look something like the
theory of constructed emotion (Barrett, 2017), formerly, the conceptual
act theory of emotion (Barrett, 2006b, 2011a, 2012, 2013,
2014).
To begin this discussion, I first outline enough background
on brain structure and function to start asking informed questions
about the biological basis of emotion. I then introduce the
theory of constructed emotion, contrast it briefly with the classical
view when instructive to do so, and consider selected
Received: 13 August 2016; Revised: 13 August 2016; Accepted: 11 October 2016
VC The Author (2016). Published by Oxford University Press. For Permissions, please email: journals.permissions@oup.com
1 Throughout the millennia, with few exceptions, cognitions were
thought to reside in the brain, emotions in the body, and then later,
emotions were relocated to the parts of the brain that control the body.
For example, Aristotle placed both thinking and feeling in organs of
the body; Descartes kept emotions in the body and placed cognition in
the pineal gland of the brain).
1
Social Cognitive and Affective Neuroscience, 2017, 1–23
doi: 10.1093/scan/nsw154
Advance Access Publication Date: 19 October 2016
Original article
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findings on the brain basis of emotion through the theory’s
lens. In the process, I offer a series of novel hypotheses about
what emotions are and how they work.
The biological background
What is a brain?
A brain is a network of billions of communicating neurons, bathed
in chemicals called neurotransmitters, which permit neurons to
pass information to one another (Doya, 2008; Bargmann, 2012). The
firing of a single neuron (or a small population of neurons) represents
the presence or absence of some feature at a moment in
time (Deneve, 2008; Deneve and Jardri, 2016). However, a given neuron
(or group of neurons) represents different features from moment
to moment (e.g. Stokes et al., 2013; Spillmann et al., 2015)
because many neurons synapse onto one (many-to-one connectivity),
and a neuron’s receptive field depends on the information it
receives (i.e. depends on its neural context in the moment;
McIntosh, 2004). Conversely, one neuron also synapses on many
Fig. 1. The classical view of emotion. The classical view of emotion includes basic emotion theories (e.g. for a review, see Tracy and Randles, 2011), causal appraisal theories
(e.g. Scherer, 2009; Roseman, 2011), and theories of emotion that rely on black-box functionalism (Davis, 1992; Anderson and Adolphs, 2014). Each emotion faculty is
assumed to have its own innate ‘essence’ that distinguishes it from all other emotions. This might be a Lockean essence (an underlying causal mechanism that all instances
of an emotion category share, making them that kind of emotion and not some other kind of emotion, depicted by the circles in the figure). Lockean essences
might be a biological, such as a set of dedicated neurons, or psychological, such as a set of evaluative mechanisms called ‘appraisals’. An emotion category is usually
assumed to have a Platonic essence [a physical fingerprint that instances of that emotion share, but that other emotions do not, such a set of facial movements (an ‘expression’),
a pattern of autonomic nervous system activity, and/or a pattern of appraisals]. Of course, no one is expecting complete invariance, but it is assumed that instances
of a category are similar enough to be easily diagnosed as the same emotion using objective (perceiver-independent) measures alone. (A) is adapted from Davis
(1992). (B) is adapted Anderson and Adolphs (2014). (C) is adapted from Barrett (2006a), which reviews the growing evidence that contracts the classical view of emotion.
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other neurons [one-to-many connectivity\ (Sporns, 2011; Sterling
and Laughlin, 2015)] to help implement instances of different psychological
categories. As a consequence, neurons are multipurpose
[for evidence and discussion, see (Barrett and Satpute, 2013;
Anderson, 2014; Anderson and Finlay, 2014)], even in subcortical regions
like the amygdala (Cerf, personal communication, 30 July
2015).2
When the brain is viewed as a massive network, rather than
a single organ or a collection of ‘mental modules’, it becomes
apparent that this one anatomic structure of neurons can create
an astounding number of spatiotemporal patterns, making the
brain a network of high complexity (Sporns, 2011; Bullmore and
Sporns, 2012; Rigotti et al., 2013). Natural selection prefers high
complexity systems as they can reconfigure themselves into a
multitude of different states (Whitacre, 2010; Whitacre and
Bender, 2010; Sterling and Laughlin, 2015).
The brain achieves complexity through ‘degeneracy’
(Edelman and Gally, 2001), the capacity for dissimilar representations
(e.g. different sets of neurons) to give rise to instances of
the same category (e.g. anger) in the same context (i.e. many-toone
mappings of structure to function). Degeneracy is ubiquitous
in biology, from the workings inside a single cell to distributed
brain networks (e.g. see Tononi et al., 1999; Edelman and
Gally, 2001; Marder and Taylor, 2011). Natural selection favors
systems with degeneracy because they are high in complexity
and robust to damage (Whitacre and Bender, 2010). Degeneracy
explains why Roger, the patient who lost his limbic circuitry to
herpes simplex type I encephalitis, still experiences emotions
(Feinstein et al., 2010) and why monozygotic twins with fully calcified
basolateral sectors of the amygdala [due to UrbachWiethe
disease (UWD)] have markedly different emotional capacity,
despite genetic and environmental similarity (Becker et
al., 2012; Mihov et al., 2013). Degeneracy also explains how a
characteristic can be highly heritable even without a single set
of necessary and sufficient genes (e.g. Turkheimer et al., 2014).
In emotion research, degeneracy means that instances of an
emotion (e.g. fear) are created by multiple spatiotemporal patterns
in varying populations of neurons. Therefore, it is unlikely
that all instances of an emotion category share a set of core features
(i.e. a single facial expression, autonomic pattern or set of
neurons; see Clark-Polner et al., 2016). This observation is an
example of population thinking, pioneered in Darwin’s On the
Origin of Species (Mayr, 2004).3
By observing the natural world,
Darwin realized that biological categories, such as a species, are
conceptual categories (highly variable instances, grouped
together by ‘a goal’ rather than by similar features or a single,
shared underlying cause; (Mayr, 2004). My hypothesis, following
Darwin’s insight, is that fear (or any other emotion) is a
‘category’ that is populated with highly variable instances
(Clark-Polner et al., 2016; Clark-Polner, Johnson & Barrett, 2016;
e.g. Wilson-Mendenhall et al., 2011, 2015). The summary
representation of any emotion category is an abstraction that
need not exist in nature (as is true for any biological category;
for a discussion of population thinking, see Mayr, 2004; as
applied to emotion concepts and categories, see Barrett, 2017;
and, as applied to concepts and categories more generally see
Barsalou, 1983; Voorspoels et al., 2011). The fact that human
brains effortlessly and automatically construct such
representations (e.g. Murphy, 2002; Posner and Keele, 1968)
helps to explain why scientists continue to believe in the
classical view and even propose it as an innovation (e.g.
Anderson and Adolphs, 2014), even as evidence continues to
call it into doubt (e.g. Barrett, 2006a, 2016b, 2012; Barrett et al.,
2007a; see Table 1 for specific neuroscience examples, with a
particular focus on fear as the category that has garnered the
most support for the classical view).
What is a brain for?
A brain did not evolve for rationality, happiness or accurate perception.
All brains accomplish the same core task (Sterling and
Laughlin, 2015): to efficiently ensure resources for physiological
systems within an animal’s body (i.e. its internal milieu) so that
an animal can grow, survive and reproduce. This balancing act
is called ‘allostasis’ (Sterling, 2012). Growth, survival and reproduction
(and therefore gene transmission) require a continual
intake of metabolic and other biological resources. Metabolic
and other expenditures are required to plan and execute the
physical movements necessary to acquire those resources in
the first place (and to protect against threats and dangers).
Allostasis is not a condition of the body, but a process for how
the brain regulates the body according to costs and benefits; ‘efficiency’
requires the ability to anticipate the body’s needs and
satisfy them before they arise (Sterling, 2012; Sterling and
Laughlin, 2015).4
An animal thrives when it has sufficient resources
to explore the world, and to consolidate the details of
2 Cells in the medial temporal lobe (including the amygdala) appear to
act as a memory cache for important things (e.g. photos of friends,
family, famous people, the patients themselves, landscapes, directions;
some cells don’t respond to anything for a few days, and then
begin to respond when the experimenters walk into the room); at
some other point, the cells might adopt and code for something entirely
different that becomes important (Cerf, personal communication,
30 July 2015). Even primary sensory neurons are not coding for
single sensory features but for associations between one feature (like
the presence or absence of a line) with other sensory features; e.g. V1
neurons have receptive fields that include auditory and sensorimotor
changes (e.g. Liang et al., 2013).
3 Before On the Origin of Species, a ‘species’ was defined as biological type
(i.e. with a set of unchanging physical characteristics or features that
are passed down through the generations). This typological characterization
fundamentally underestimates within-category variation (in its
phenotypic features and in it’s gene pool) and over-estimates between
category variation (and borderline cases are often encountered; Mayr,
2004; Gelman and Rhodes, 2012). One of Darwin’s greatest conceptual
innovations in Origin was to revolutionize the concept of a species as a
biopopulation of highly variable individuals (instead of a group of
highly similar creatures who share a set of co-occurring biological
features) (Mayr, 2004). Since then, the concept of a ‘species’ has been
characterized on the basis of what category members do (i.e. functionally),
not on the basis of a shared gene pool or a set of physical features:
A species is a reproductive community (sometimes, members of
different species are reproductively incompatible; sometimes they
don’t, such as when they are geographically isolated). Fundamentally,
this translates into the insight that a biological category (a ‘species’) is
a conceptual category, rather than a typological one: a species is a
population of physically unique individuals who similarities are
defined functionally, not physically.
4 Sometimes allostasis involves dynamically regulating resource allocation
(i.e. diverting glucose, electrolytes, water, etc. from one system to
another) to meet the body’s spending needs; e.g. in advance of standing
up, the heart beats stronger and faster, blood vessels constrict, and
blood pressure raises to ensure that the brain continues to receive the
blood (and oxygen). Sometimes allostasis involves signaling the need
for resources before the body runs out ( e.g. drinking before dehydration
occurs) or preparing for the intake of resources in advance of their
ingestion; e.g. saliva example in humans and some other mammals,
saliva is made of alpha-amylase which is an enzyme that breaks down
glucose. When the body is in need of glucose, saliva is pre-emptively
secreted (even before anything is ingested). Even just imaging food
causes glucose secretion.
L. F. Barrett | 3
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Table 1. Examples of neuroscience evidence that disconfirm the classical view of emotion
Observation Method Example Citations
Different emotion categories cannot be specifically and consistently localized
to distinct populations of neurons within a single region of the human
brain.
Human neuroimaging:
task-related data
(Vytal and Hamann, 2010;
Lindquist et al., 2012)
Different emotion categories cannot be consistently localized to specific intrinsic
networks in the human brain.
Human neuroimaging: intrinsic
connectivity data
(Barrett and Satpute, 2013;
Touroutoglou et al., 2015)
The instances of an emotion category need not share a population of neurons
that are necessary or sufficient to implement them.
Human neuroimaging:
multi-voxel pattern
analysis
(Clark-Polner, Johnson, &
Barrett, 2016)
Individual neurons, when stimulated in studies of experience, expression,
and perception, do not have emotion-specific receptive fields.
Intracranial stimulation in
humans
(Guillory and Bujarski, 2014)
Lesions to the amygdala produce variable functional consequences.
Monozygotic twins, whose basolateral nuclei of both amygdalae are calcified
due to UWD, do not show equivalent deficits in experiencing and perceiving
fear; patient BG has deficits similar to patient SM (who has
complete loss of both amygdalae due to UWD), whereas her sister, AM, is
able to experience and perceive fear when BG cannot. Other people with
basolateral lesions from UWD show different problems in fear perception
(they are vigilant to rather than neglectful of posed fear faces). Patient SM
can experience intense fear in the real world under certain circumstances,
and her impairments in fear perception appear to be limited to experiments
where she is asked to view stereotyped, fear poses and explicitly
categorize them as fearful. There is ample evidence that she is able to perceive
fear in various circumstances in real life (see Box 1).
Behavioral observations in
humans with amygdala
lesions
(Bechara et al., 1995, 1999;
Adolphs et al., 1999;
Adolphs and Tranel,
1999, 2003; Atkinson
et al., 2007; de Gelder
et al., 2014; Hampton
et al., 2007; Tsuchiya
et al., 2009; Hurlemann
et al., 2007; De Martino
et al., 2010; Boes et al.,
2011; Feinstein et al.,
2011, 2013, 2016; Becker
et al., 2012; Terburg et al.,
2012; Feinstein, 2013;
Mihov et al., 2013)
Various circuits acting in parallel or collaboratively support learning when to
perform behaviors that are typically referred to as ‘fear behaviors’. Some
have argued that these circuits represent distinct pathways from the
amygdala to the periaqueductal gray through the hypothalamus to control
different situation-specific fear behaviors, but others find that there are
many (circuits) to one (behavior) mappings. Others find one (circuit) to
many (behavior) mappings. Still others find that the amygdala, or specific
parts (e.g. the basolateral nuclei), are not necessary for the expression of
previously learned aversive responses (i.e. the way that learning is expressed
depends on the context and the available options for behavior).
Also, cortical regions (e.g. dmPFC and vmPFC) appear necessary for aversive
learning when the context is more ecologically valid and less artificially
simple. One thing is certain: scientists routinely engage in mental
inference and refer to circuits as controlling different types of fear when in
fact they are studying context-dependent behaviors that may not bear a
one-to-one correspondence to fear.
Optogenetic research and
some lesion research in
rodents
(Furlong et al., 2010; Gross
and Canteras, 2012; Herry
and Johansen, 2014;
Sharpe and Killcross,
2015; Tovote et al., 2015;
McGaugh, 2016)
The expression of aversive learning depends on the state of the animal. For
example, when the conditioned stimulus (a tone) is presented alone after
having been paired with the unconditioned stimulus (an electric shock),
the animal typically freezes, its heart rate increases, and its skin conductance
goes up, which is usually taken as evidence that the animal has
learned fear. Yet when an animal is restrained in position as it hears the
tone, its heart rate decreases.
Classical conditioning in
rats
(Iwata and LeDoux, 1988)
Adult monkeys with amygdala lesions are more likely to explore novel objects
right away (which is usually interpreted as a ‘lack of fear’) but an alternative
explanation is that the amygdala helps to regulate exploratory
behavior in novel situations, which in turn will increase sensory processing
when there is substantial prediction error. ‘Fear’ is not necessary. An
amygdala might be required for aversive learning, but not the behavioral
response learned (paralleling observations in rodent experiments).
Lesions in non-human
primates
(Mason et al., 2006;
Antoniadis et al., 2009)
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experience within the brain’s synaptic connections, making
those experiences available to guide later decisions about future
expenditures and deposits. Too much of a resource (e.g. obesity
in mammals) or not enough (e.g. fatigue, Dantzer et al., 2014) is
suboptimal. Prolonged imbalances can lead to illness (e.g.
Hunter and McEwen, 2013; McEwen et al., 2015) that remodels
the brain (Crossley et al., 2014; Goodkind et al., 2015) and the
sympathetic nervous system, with corresponding behavior
changes (Sloan et al., 2007; Capitanio and Cole, 2015; for a review,
see Sloan et al., 2008).
Whatever else your brain is doing—thinking, feeling, perceiving,
emoting—it is also regulating your autonomic nervous
system, your immune system and your endocrine system as resources
are spent in seeking and securing more resources. All
animal brains operate in the same manner (i.e. even insect
brains coordinate visceral, immune and motor changes; Sterling
and Laughlin, 2015, p. 91). This regulation helps explain why, in
mammals, the regions that are responsible for implementing
allostasis (the amygdala, ventral striatum, insula, orbitofrontal
cortex, anterior cingulate cortex, medial prefrontal cortex
(mPFC), collectively called ‘visceromotor regions’) are usually
assumed to contain the circuits for emotion. In fact, many of
these visceromotor regions are some of the most highly
connected regions in the brain, and they exchange information
with midbrain, brainstem, and spinal cord nuclei that coordinate
autonomic, immune, and endocrine systems with one another,
as well as with the systems that control skeletomotor
movements and that process sensory inputs. Therefore these
regions are clearly multipurpose when it comes to constructing
the mental events that we group into mental categories
(see Figure 2).
How does a brain perform allostasis?
For a brain to effectively regulate its body in the world, it runs
an internal model of that body in the world.5
In psychology, we
refer to this modeling as ‘embodied simulation’ (Barsalou, 2008;
Barsalou et al., 2003) (e.g. see Figure 3). An internal model is
metabolic investment, implemented by intrinsic activity (e.g.
Fig. 2. Hubs in the human brain. (A) Hubs of the rich club, adapted from van den Heuvel and Sporns (2013). These regions are strongly interconnected with one another and it is
proposed that they integrate information across the brain to create large-scale patterns of information flow (i.e. synchronized activity; van den Heuvel and Sporns, 2013). They are
sometimes referred to as convergence or confluence zones (e.g. Damasio, 1989; Meyer and Damasio, 2009). (B) Results of a forward inference analysis, revealing ‘hot spots’ in the
brain that show a better than chance increase in BOLD signal across 5633 studies from the Neurosynth database. Activations are thresholded at FWE P < 0.05. Limbic regions (i.e.
agranular/dysgranular with descending projections to visceromotor control nuclei) include the cingulate cortex [midcingulate cortex (MCC), pregenual anterior cingulate cortex
(pgACC)], ventromedial prefrontal cortex (vmPFC), supplementary motor and premotor areas (SMA and PMC), medial temporal lobe, the anterior insula (aINS) and ventrolateral prefrontal
cortex (vlPFC) (e.g. Carrive and Morgan, 2012; Bar et al., 2016); for a discussion and additional references, see (Kleckner et al., in press). AG, angular gyrus; MC, motor cortex.
5 There is a well-known principle of cybernetics: anything that regulates
(i.e. acts on) a system must contain an ‘internal model’ of that system
(Conant and Ross Ashby, 1970). From a brain’s perspective, the ‘system’
in question includes it’s body and it’s ecological niche; a body must be
watered, fed and cared for, so that a creature can grow, thrive, and ultimately,
reproduce and care for it’s young so as to pass its genes to
the subsequent generation.
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Berkes et al., 2011) that, in humans, occupies 20% of our total energy
consumed (Raichle, 2010).6
Given these considerations,
modeling the world ‘accurately’ in some detached, disembodied
manner would be metabolically reckless. Instead, the brain
models the world from the perspective of its body’s physiological
needs.7
As a consequence, a brain’s internal model includes
not only the relevant statistical regularities in the
extrapersonal world, but also the statistical regularities of the
internal milieu. Collectively, the representation and utilization
of these internal sensations is called ‘interoception’ (Craig,
2015). Recent research suggests that interoception is at the core
of the brain’s internal model and arises from the process of allostasis
(Barrett and Simmons, 2015; Chanes and Barrett, 2016;
Barrett, 2017; for related discussions, see Seth et al., 2012; Seth,
2013; Pezzulo et al., 2015; Seth & Friston, 2016). Interoceptive
sensations are usually experienced as lower dimensional feelings
of affect (Barrett and Bliss-Moreau, 2009; Barrett, 2017). As
such, the properties of affect—valence and arousal (Barrett and
Russell, 1999; Kuppens et al., 2013)—are basic features of consciousness
(Damasio, 1999; Dreyfus and Thompson, 2007;
Edelman and Tononi, 2000; James, 1890/2007; Searle, 1992, 2004;
Wundt, 1897) that, importantly, are not unique to instances of
emotion.
All animals run an internal model of their world for the purpose
of allostasis (i.e. the notion of an internal model is speciesgeneral).
Even single-celled organisms that lack a brain learn,
remember, make predictions, and forage in service to allostasis
(Freddolino and Tavazoie, 2012; Sterling and Laughlin, 2015).
The content of any internal model is species-specific, however,
including only the parts of the animal’s physical surroundings
that its brain has judged relevant for growth, survival and reproduction
(i.e. a brain creates its affective niche in the present
based on what has been relevant for allostasis in the past).
Everything else is an extravagance that puts energy regulation
at risk.
As an animal’s integrated physiological state changes constantly
throughout the day, its immediate past determines the
aspects of the sensory world that concern the animal in the present,
which in turn influences what its niche will contain in the
immediate future. This observation prompts an important insight:
neurons do not lie dormant until stimulated by the outside
world, denoted as stimulus!response.8
Ample evidence
shows that ongoing brain activity influences how the brain
processes incoming sensory information (e.g. Sayers et al.,
1974),9
and that neurons fire intrinsically within large networks
without any need for external stimuli (Swanson, 2012). The implications
of these insights are profound: namely, it is very unlikely
that perception, cognition, and emotion are localized in
dedicated brain systems, with perception triggering emotions
that battle with cognition to control behavior (Barrett, 2009).
This means classical accounts of emotion, which rely on this
S!R narrative, are highly doubtful.
An internal model is predictive, not reactive
An increasingly popular hypothesis is that the brain’s simulations
function as Bayesian filters for incoming sensory input,
driving action and constructing perception and other psychological
phenomena, including emotion. Simulations are thought
to function as prediction signals (also known as ‘top-down’ or
‘feedback’ signals, and more recently as ‘forward’ models) that
continuously anticipate events in the sensory environment.10
Fig. 3. Neural activity during simulation. N ¼ 16 (data from Wilson-Mendenhall et al., 2013). Participants listened with eyes closed to multimodal descriptions rich in
sensory details and imagined each real-world scenario as if it was actually happening to them (i.e. the experiences were high in subjective realism). Contrast presented
is scenario immersion > resting baseline; maps are FDR corrected P < 0.05. Left image, x ¼ 1; right image, x ¼ À42. Heightened neural activity in primary visual cortex
(not labeled), somatosensory cortex (SSC), and MC during scenario immersion replicated prior simulation research (McNorgan, 2012) and established the validity of the
paradigm. Notice that simulation was associated with an increase in BOLD response within primary interoceptive cortex (i.e. the pINS), in the sensory integration network
of lateral orbitofrontal cortex (lOFC) (Ongur et al., 2003) and in the thalamus; increased BOLD responses were also seen, as expected, in limbic and paralimbic regions
such as the vmPFC, the aINS, the temporal pole (TP), SMA and vlPFC, as well as in the hypothalamus and the subcortical nuclei that control the internal milieu.
PAG, periacquiductal gray; PBN, parabrachial nucleus.
6 Long-range neural connections, like those that form the human brain’s
broadly distributed intrinsic networks, are particularly expensive
(Bullmore and Sporns, 2012; Sterling and Laughlin, 2015), with most of
the energy costs going to signaling between neurons, particularly in
post-synaptic processes (Attwell and Laughlin, 2001; Attwell and
Iadecola, 2002; Alle et al., 2009; Harris et al., 2012).
7 A trivial example, of course, is that infrared light is not normally something
a human can see and so your brain (and mine) does not normally
represent it. In this regard, we humans have been able to expand our
ecological niche (and therefore our internal models) with technology.
8 This mistaken belief is an artifact of studying neurons in isolation (e.g.
Hodgkin and Huxley, 1952), which creates a misleading picture of how
the nervous system functions (Marder, 2011). For a similar view, see
(Dewey, 1896).
9 Also see Makeig et al., 2002, 2004; Mazaheri and Jensen, 2010;
Laxminarayan et al., 2011; Qian and Di, 2011; Scheeringa et al., 2011.
10 The term ‘feedback’ derives from a time when the brain was thought
to be largely stimulus driven (Sartorius et al., 1993). Nonetheless, the
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This hypothesis is variously called predictive coding, active inference,
or belief propagation (e.g. Rao and Ballard, 1999;
Friston, 2010; Seth et al., 2012; Clark, 2013a,b; Hohwy, 2013; Seth,
2013; Barrett and Simmons, 2015; Chanes and Barrett, 2016;
Deneve and Jardri, 2016).11
Without an internal model, the brain
cannot transform flashes of light into sights, chemicals into
smells and variable air pressure into music. You’d be experientially
blind (Barrett, 2017). Thus, simulations are a vital ingredient
to guide action and construct perceptions in the present.12
They are embodied, whole brain representations that anticipate
(i) upcoming sensory events both inside the body and out as
well as (ii) the best action to deal with the impending sensory
events. Their consequence for allostasis is made available in
consciousness as affect (Barrett, 2017).
I hypothesize that, using past experience as a guide, the
brain prepares multiple competing simulations that answer the
question, ‘what is this new sensory input most similar to?’ (see
Bar, 2009a,b). Similarity is computed with reference to the current
sensory array and the associated energy costs and potential
rewards for the body. That is, simulation is a partially
completed pattern that can classify (categorize) sensory signals
to guide action in the service of allostasis. Each simulation has
an associated action plan. Using Bayesian logic (Deneve, 2008;
Bastos et al., 2012), a brain uses pattern completion to decide
among simulations and implement one of them (Gallivan et al.,
2016), based on predicted maintenance of physiological efficiency
across multiple body systems (e.g. need for glucose, oxygen,
salt etc.).
From this perspective, unanticipated information from the
world (prediction error) functions as feedback for embodied simulations
(also known as ‘bottom-up’ or, confusingly, ‘feedforward’
signals). Error signals track the difference between the predicted
sensations and those that are incoming from the sensory world
(including the body’s internal milieu). Once these errors are minimized,
simulations also serve as inferences about the causes of
sensory events and plans for how to move the body (or not) to deal
with them (Lochmann and Deneve, 2011; Hohwy, 2013). By modulating
ongoing motor and visceromotor actions to deal with upcoming
sensory events, a brain infers their likely causes.
In predictive coding, as we will see, sensory predictions arise
from motor predictions; simulations arise as a function of visceromotor
predictions (to control your autonomic nervous system,
your neuroendocrine system, and your immune system)
and voluntary motor predictions, which together anticipate and
prepare for the actions that will be required in a moment from
now. These observations reinforce the idea that the stimulus!response
model of the mind is incorrect.13
For a given
event, perception follows (and is dependent on) action, not the
other way around. Therefore, all classical theories of emotion
are called into question, even those that explain emotion as iterative
stimulus !response sequences.
The computational architecture of the brain is a
conceptual system plus pattern generators
The mechanistic details of predictive coding provide yet another
deep insight: a brain implements its internal model with
‘concepts’ that ‘categorize’ sensations to give them meaning
(Barrett, 2017).14
Predictions are concepts (see Figure 4).
Completed predictions are categorizations that maintain
physiological regulation, guide action and construct perception.
The meaning of a sensory event includes visceromotor and
motor action plans to deal with that event. As detailed in Figure
5, meaning does not trigger action, but results from it. This
makes classical appraisal theories highly doubtful, because they
assume that a response derives from a stimulus that is evaluated
for its meaning (e.g. Lazarus, 1991; Scherer, 2009;
Roseman, 2011; for a discussion, see (Barrett et al., 2007b; Gross
and Barrett, 2011). Appraisals as descriptions of the world (e.g.
Clore and Ortony, 2008), however, are produced by categorization
with concepts (e.g. Si et al., 2010).
Traditionally, a ‘category’ is a population of events or objects
that are treated as similar because they all serve a particular
goal in some context; a ‘concept’ is the population of representations
that correspond to those events or objects.15
I
history of science is laced with the idea that the mind drives perception
[e.g. in the 11th century by Ibn al-Haytham who helped to invent
the scientific method, in the 18th century by Kant (1781), and in the
19th century by Helmholtz]. In more modern times, see Craik’s concept
of internal models (1943), Tolman’s cognitive maps (1948),
Johnson-Laird’s internal models, and for more recent references,
Neisser (1967) and Gregory (1980). The novelty in recent formulations
can be found in (i) the hypothesis that predictions are ‘embodied’
simulations of sensory-motor experiences, (ii) they are ultimately in
the service of allostasis and therefore interoception is at their core
and, of course (iii) the breadth of behavioral, functional, and anatomic
evidence supporting the hypothesis that the brain’s internal model
implements active inference as prediction signals, including (iv) the
specific computational hypotheses implementing a predictive coding
account.
11 Notably, Buzsaki (2006) wrote that ‘Brains are foretelling devices’.
There is accumulating evidence that prediction and prediction error
signals oscillate at different frequencies within the brain (e.g. Arnal
and Giraud, 2012; Bressler and Richter, 2015; Brodski et al., 2015).
12 Simulations also constitute representations of the past (i.e. memories) and
the future (i.e. prospections), and implement imagination, mind wandering,
and daydreams (Schacter et al., 2007; Buckner et al., 2008).
13 For an excellent treatment of the conceptual baggage in words like
‘organism’, ‘stimulus’ and ‘response’, see Danziger (1997); in particular,
see the thoughtful historical discussion of how motives and emotions
became conceptualized as sources of ‘internal’ stimulation and
how physiological changes became ‘responses’ to that stimulation.
14 For those who are unfamiliar with predictive coding, consider the
problem of allostasis from the perspective of your own brain. For your
entire life, your brain is entombed in a dark, silent box (i.e. a skull). It
has to figure out the causes of sensory events outside your skull to
guide action in the service of allostasis, but all it has access to their
consequences in the form of sights, sounds, smells, touches, tastes
and interoceptive sensations (i.e. sensations from your heart pumping,
your lungs expanding, from inflammation, from metabolic processes
and so on). So, your brain is faced with a problem of reverse
inference: any given sensation—a flash of light or a sound or an ache
or cramp—can have many different causes. In addition, the sensory
information is dynamically changing, noisy, and ambiguous. Your
brain solves this puzzle by using the only other source of information
available to it—past experiences—to create simulations that predict
incoming sensory events before their consequences arrive to the
brain. In this way, your brain efficiently uses the statistical regularities
from its past to anticipate future events that must be dealt with.
15 Traditionally, categories are supposed to exist in the world, whereas
concepts are supposed to exist in the brain. This distinction makes
sense for natural kind categories (where the boundaries exist independent
of perceivers) or when the instances of a category share
physical similarities – some set of statistical regularities in their sensory
aspects or perceptual features (e.g., most human faces have a
certain set of visual features – two eyes, two ears, a nose, some hair,
and a mouth – in approximately the same orientation). In many
cases, however, the boundary between a category and its concept is
blurred. For example, consider a category whose instances share a
similar function, but do not share any physical features (e.g., currency
throughout the course of human history). These conceptual
L. F. Barrett | 7
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Fig. 4. The brain is a concept generator. (A) Brodmann areas are shaded to depict their degree of laminar organization, including the insula (bottom right). The brain’s
computational architecture is depicted (adapted from Barbas, 2015), where prediction signals flow from the deep layers of less granular regions (cell bodies depicted
with triangles) to the upper layers of more granular regions; this, can also be thought of concept construction [as described in Barrett (2017)]. I hypothesize that agranular
(i.e. limbic) cortices generatively combine past experiences to initiate the construction of embodied concepts; multimodal summaries cascade to sensory and motor
systems to create the simulations that will become motor plans and perceptions. Prediction error processing, in turn, is akin to concept learning. The upper layers of
cortex compress prediction errors and reduce error dimensionality, eventually creating multimodal summaries, by virtue of a cytoarchitectural gradient: prediction
error flows from the upper layers of primary sensory and motor regions (highly granular cortex) populated with many small pyramidal cells with few connections towards
less granular heteromodal regions (including limbic cortices) with fewer but larger pyramidal cells having many connections (Finlay and Uchiyama, 2015). (B)
Evidence of conceptual processing in the default mode network: Multimodal summaries for emotion concepts [adapted from Skerry and Saxe (2015), Figure 1B]; summary
representations of sensory-motor properties (color, shape, visual motion, sound and physical manipulation [Fernandino et al. (2016), Figure 5]; and, semantic processing
[adapted from Binder and Desai (2011), Figure 2]. (C) Regions that consistently increase activity during emotional experience (green), emotion regulation (blue),
and their overlap (red) [as appears in Clark-Polner et al. (2016); adapted from Buhle et al. (2014) and Satpute et al. (2015)]. Overlaps are observed in the aIns, vlPFC, the
MCC, SMA and posterior superior temporal sulcus. Studies of emotional experience show consistent increase in activity that is consistent with manipulating predictions
(i.e. the default mode and salience networks), whereas reappraisal instructions appear to manipulate the modification of those predictions (i.e. the frontoparietal
and salience networks). (D) Intensity maps for five emotion categories examined by Wager et al. (2015). Maps represent the expected activations or population centers,
given a specific emotion category. Maps also reflect expected co-activation patterns. Notice that population centers for all emotion categories can be found within the
default mode and salience networks. These are probabilistic summaries, not brain states for emotion Adapted from Wager et al. (2015).
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hypothesize that in assembling populations of predictions, each
one having some probability of being the best fit to the current
circumstances (i.e., Bayesian priors), the brain is constructing
concepts (Barrett, 2017) or what Barsalou refers to as ‘ad hoc’
concepts (Barsalou, 1983, 2003; Barsalou et al., 2003). In the language
of the brain, a concept is a group of distributed ‘patterns’
of activity across some population of neurons. Incoming sensory
evidence, as prediction error, helps to select from or modify
this distribution of predictions, because certain simulations will
better fit the sensory array (i.e. they will have stronger priors),
with the end result that incoming sensory events are categorized
as similar to some set of past experiences. This, in effect,
is the original formulation of the conceptual act theory of emotion
(see Barrett, 2006b, 2017): the brain uses emotion concepts
to categorize sensations to construct an instance of emotion.
That is, the brain constructs meaning by correctly anticipating
(predicting and adjusting to) incoming sensations. Sensations
are categorized so that they are (i) actionable in a situated way
and therefore (ii) meaningful, based on past experience. When
past experiences of emotion (e.g. happiness) are used to categorize
the predicted sensory array and guide action, then one
experiences or perceives that emotion (happiness).
In other words, an instance of emotion is constructed the
same way that all other perceptions are constructed, using the
same well-validated neuroanatomical principles for information
flow within the brain. Barbas and colleagues’ structural
model of corticocortical connections (Barbas and RempelClower,
1997; Barbas, 2015) provides specific hypotheses about
how concepts categorize incoming sensory inputs to guide action
and create perception, and in doing so fills the computational
and neural gaps in my initial theoretical formulation of
the theory, providing novel hypotheses about how a brain constructs
emotional events [outlined in Barrett and Simmons
(2015) and Chanes and Barrett (2016), Barrett (2017)]. The first
key observation is that prediction signals are carried via ‘feedback’
connections that originate in cortical regions with the
least well-developed laminar structure, referred to as ‘agranular’.
Agranular regions are cytoarchitecturally arranged to send
but not receive prediction signals within the cerebral cortex.
Another name for agranular cortices is ‘limbic’. Limbic cortices,
such as the anterior cingulate cortex and the ventral portion of
the anterior insula (aINS), allostatically control physiology by relaying
descending prediction signals to the internal milieu via a
system of subcortical regions (Bar et al., 2016; Kleckner et al., in
press), including the central nucleus of the amygdala
(Ghashghaei et al., 2007), the ventral and dorsal striatum, and
the central pattern generators (Swanson, 2012) across hypothalamus,
the parabrachial nucleus, periaqueductal grey, and the
solitary nucleus (see Figure 5A and B). Cortical regions with a
dysgranular structure, which are referred to as limbic (Barbas,
2015) or paralimbic (Mesulam, 1998), also issue descending prediction
signals to the body’s internal milieu [e.g. midcingulate
cortex, mPFC (MCC), ventrolateral prefrontal cortex (vlPFC), premotor
cortex (PMC), etc., see Figure 5A and B]. My hypothesis is
that these ‘visceromotor’ regions of the brain that are responsible
for implementing allostasis, and that are usually assigned
an emotional function, are ‘driving’ the perception signals, i.e.
the ‘concepts’, that constitute the brain’s internal model, in
conjunction with the hippocampus (e.g. see Davachi and
DuBrow, 2015; Hasson et al., 2015).
A concept is not only the descending prediction signals that
control the viscera. It also includes the efferent copies of those
signals that cascade to primary motor cortex (MC) as skeletomotor
prediction signals, as well as to all primary sensory cortices
as sensory prediction signals (see Figure 5C and D, respectively;
for a discussion, see Bastos et al., 2012; Adams et al., 2013;
Barbas, 2015; Barrett and Simmons, 2015; Chanes and Barrett,
2016). Following the evidence for how the cytoarchitectural gradients
in the cortical sheet predict information flow across cortical
regions (Barbas et al., 1997, p. 6608), prediction signals flow
from deep layers of limbic cortices and terminate in the upper
layers of cortical regions with more developed (i.e. more granular)
structure, such as gustatory and olfactory cortex, primary
MC, primary interoceptive cortex, and the primary visual, auditory
and somatosensory regions.16
Because MC has a laminar organization that is less well developed
than primary visual, auditory, somatosensory and interoceptive
sensory regions (Barbas and Garcıa-Cabezas, 2015), I
hypothesize that MC sends efferent copies to those sensory regions
as sensory predictions (see Figure 5D, red lines). A similar
arrangement between motor and somatosensory cortex has
been proposed by Friston and colleagues (Adams et al., 2013).
Furthermore, because of their differential laminar development,
I hypothesize that primary interoceptive cortex in mid-toposterior
dorsal insula forwards sensory predictions to visual,
auditory and somatosensory cortices (propagating across either
a single or multiple synapses; Figure 5D, gold lines). The skeletomotor
prediction signals prepare the body for movement, the
interoceptive prediction signals initiate a change in affect (i.e.
the expected sensory consequences of allostatic changes within
the body’s internal milieu), and the extrapersonal sensory prediction
signals prepare upcoming perceptions. This hypothesis
is consistent not only with over three decades of tract tracing
studies in non-human animals, but also with engineering design
principles (i.e. compute locally, and relay only the information
that is needed to assemble a larger pattern; Sterling and
Laughlin, 2015). Predictions literally change the firing of primary
sensory and motor neurons, even though the incoming sensory
input has not yet arrived (and may never arrive; e.g. Kok et al.,
2016). Accordingly, all action and perception are created with
concepts. All concepts contribute to allostasis and represent
changes in affect, not just those that construct the events that
feel affectively intense or are created with emotion concepts.
To consider how this works, try this thought experiment: in
the past, you have experienced diverse instances of happiness,
may be lying outdoors on a sunny day, finishing a strenuous
workout, hugging a close friend, eating a piece of delectable
chocolate or winning a competition. Each instance is different
from every other, and when the brain creates a concept of happiness
to categorize and make sense of the upcoming sensory
categories have also been called abstract or nominal categories.
Biological categories are conceptual categories, as we learned in On
the Origin of Species. The categories of social reality, such as flowers
and weeds, or emotion categories, are conceptual because functions
are imposed on physically disparate instances by virtual of collective
agreement (Barrett, 2012).
16 Primary visual, auditory, and somatosensory cortices have the most
developed laminar structure within the cerebral cortex and therefore
receive prediction signals but are unable to send them. Primary interoceptive
cortex is relatively less developed than these regions, and
therefore sends multimodal sensory predictions to these exteroceptive
regions. Primary motor cortex (with a small granular layer;
(Barbas and Garcıa-Cabezas, 2015) has an even less well-developed
laminar structure and therefore sends predictions to somatosensory
cortex (Adams et al., 2013; Shipp et al., 2013) as well as all the primary
sensory regions mentioned so far. Agranular limbic cortices send, but
do not receive prediction signals, because they have the least welldeveloped
laminar structure of the entire cortical mantle.
L. F. Barrett | 9
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A
B
C
D
Fig. 5. A depiction of predictive coding in the human brain. (A) Key limbic and paralimbic cortices (in blue) provide cortical control the body’s internal milieu. Primary
MC is depicted in red, and primary sensory regions are in yellow. For simplicity, only primary visual, interoceptive and somatosensory cortices are shown; subcortical
regions are not shown. (B) Limbic cortices initiate visceromotor predictions to the hypothalamus and brainstem nuclei (e.g. PAG, PBN, nucleus of the solitary tract) to
regulate the autonomic, neuroendocrine, and immune systems (solid lines). The incoming sensory inputs from the internal milieu of the body are carried along the
vagus nerve and small diameter C and Ad fibers to limbic regions (dotted lines). Comparisons between prediction signals and ascending sensory input results in prediction
error that is available to update the brain’s internal model. In this way, prediction errors are learning signals and therefore adjust subsequent predictions. (C)
Efferent copies of visceromotor predictions are sent to MC as motor predictions (solid lines) and prediction errors are sent from MC to limbic cortices (dotted lines). (D)
Sensory cortices receive sensory predictions from several sources. They receive efferent copies of visceromotor predictions (black lines) and efferent copies of motor
predictions (red lines). Sensory cortices with less well developed lamination (e.g. primary interoceptive cortex) also send sensory predictions to cortices with more
well-developed granular architecture (e.g. in this figure, somatosensory and primary visual cortices, gold lines). For simplicity’s sake, prediction errors are not depicted
in panel D. sgACC, subgenual anterior cingulate cortex; vmPFC, ventromedial prefrontal cortex; pgACC, pregenual anterior cingulate cortex; dmPFC, dorsomedial prefrontal
cortex; MCC, midcingulate cortex; vaIns, ventral anterior insula; daIns, dorsal anterior insula and includes ventrolateral prefrontal cortex; SMA, supplementary
motor area; PMC, premotor cortex m/pIns, mid/posterior insula (primary interoceptive cortex); SSC, somatosensory cortex; V1, primary visual cortex; and MC, motor
cortex (for relevant neuroanatomy references, see Kleckner et al., in press).
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events, it constructs a population of simulations (as potential
actions and perceptions) according to the rules of Bayes’
Theorem, whose priors reflect their similarity to the current
situation (before the evidence is taken into account). The similarity
need not be perceptual—it can be goal-based. So the brain
constructs an on-line concept of happiness, not in absolute
terms, but with reference to a particular goal in the situation (to
be with friends, to enjoy a meal, to accomplish a task), all in the
service of allostasis. This implies that ‘happiness’ has a specific
meaning, but its specific meaning changes from one instance to
the next.
As prediction signals cascade across the synapses of a brain,
incoming sensory signals arriving to the brain (i.e. from the external
environment and the internal periphery) simultaneously
allow for computations of prediction error that are encoded to
update the internal model (correcting visceromotor and motor
action plans, as well as sensory representations; see Figure 5,
dotted lines). Viscerosensory prediction errors arise from
physiologic changes within the internal milieu and ascend via
vagal and small diameter afferents in the dorsal horn of the spinal
cord, through the nucleus of the solitary tract, the parabrachial
nucleus, the periaqueductal gray and finally to the ventral
posterior thalamus, before arriving in granular layer IV of the
primary interoceptive insular cortex (Damasio and Carvalho,
2013; Craig, 2015). Notice that, in the context of this framework,
perception (i.e. the ‘meaning’ of sensory inputs) is constructed
with reference to allostasis, and sensory prediction errors are
treated, at a very basic level, as information that guides a ‘predicted’
visceromotor and motor action plan.
Prediction errors also arise within the amygdala, the basal
ganglia, and the cerebellum and are forwarded to the cortex to
correct its internal model (see (Beckmann et al., 2009; Buckner
et al., 2011; Haber and Behrens, 2014; Kleckner et al., in press).
I hypothesize that information from the amygdala to the cortex
is not ‘emotional’ per se, but signals uncertainty (Whalen, 1998)
about the predicted sensory input (via the basolateral complex)
and helps to adjust allostasis (via the central nucleus) as a re-
sult.17
The arousal signals that are associated with increases in
amygdala activity (e.g. Wilson-Mendenhall et al., 2013) can be
considered a learning signal (Li and McNally, 2014). Similarly,
prediction errors from the ventral striatum to the cortex
(referred to as ‘reward prediction errors; Schultz, 2016) convey
information about sensory inputs that impact allostasis more
than expected (i.e. that this information should be encoded and
consolidated in the cortex, and acted upon in the moment).
Dopamine is associated with engaging in vigorous action and
learning that is necessary to achieve the rewards that maintain
efficient allostasis (or restore it in the event of disruption), rather
than playing a necessary or sufficient role in rewards
themselves (Salamone and Correa, 2012; Guitart-Masip et al.,
2014). Other neuromodulators, such as opioids, seem to be more
intrinsic to reward in that regard (e.g. Fields and Margolis, 2015).
The cerebellum models prediction errors from the periphery
and relays them to cortex to modify motor predictions [i.e. it
predicts the sensory consequences of a motor command much
faster than actual sensory prediction errors can manage,
(Shadmehr et al., 2010), and helps the cortex reduce the sensory
consequences caused by one’s own movements]. The same
may be true for visceromotor predictions, given the connectivity
between the cerebellum and the cingulate cortex, hypothalamus
and amygdala (Schmahmann and Pandya, 1997; Strick
et al., 2009; Schmahmann, 2010; Buckner et al., 2011).18
This
would give the cerebellum a major role in allostasis, concept
generation, and the construction of emotion (e.g. see metaanalytic
evidence in Kober et al., 2008; Lindquist et al., 2012;
Wager et al., 2015).
A brain implements an internal model of the world with
concepts because it is metabolically efficient to do so. Even before
birth, a brain begins to build its internal model by processing
prediction error from the body and the world (see Barrett,
2017 for discussion). Prediction errors (i.e. unanticipated sensory
inputs) cascade in a feedforward cortical sweep, originating
in the upper layers of cortices with more developed laminar
organization and terminating in the deep layers of cortices with
less well-developed lamination. As information flows from sensory
regions (whose upper layers contain many smaller pyramidal
neurons with fewer connections) to limbic and other
heteromodal regions in frontal cortex (whose upper layers contain
fewer but larger pyramidal neurons with many more connections,
see Figure 4A), it is compressed and reduced in
dimensionality (Finlay and Uchiyama, 2015). This dimension reduction
allows the brain to represent a lot of information with a
smaller population of neurons, reducing redundancy and
increasing efficiency, because smaller populations of neurons
are summarizing statistical regularities in the spiking patterns
in larger populations with in the sensory and motor regions.
Additional efficiency is achieved because conceptually similar
representations reuse neural populations during simulation
(e.g. Rigotti et al., 2013). As a result, different predictions are separable,
but are not spatially separate (i.e. multimodal summaries
are organized in a continuous neural territory that reflects
their similarity to one another). Therefore, the hypothesis is
that all new learning (e.g. the processing of prediction error) is
concept learning, because the brain is condensing redundant
firing patterns into more efficient (and cost-effective) multimodal
summaries. This information is available for later use by
limbic cortices as they generatively initiate prediction signals,
constructed as low-dimensional, multimodal summaries (i.e.
‘abstractions’); these summaries, consolidated from prior
encoding of prediction errors, become more detailed and particular
as they propagate out to more architecturally granular
sensory and motor regions to complete embodied concept
generation.
Taking a network perspective
In a keynote address in 2006, I first proposed that several of the
brain’s intrinsic networks (what would come to be called the default
mode, salience, and frontoparietal control networks) are
domain-general or multi-use networks that are involved in constructing
emotional episodes (e.g. see Figure 6 in Kober et al.,
2008). Building on the findings so far, as well as the anatomical
distribution of limbic cortices within the brain (see Figure 5), I
17 Even more interestingly, there is some evidence to suggest that the
cortical regions projecting to the brainstem nuclei which originate
these neuromodulators (such as the locus coeruleus for norepinephrine)
are largely entrained by limbic cortical regions via descending
visceromotor predictions that project directly from the anterior cingulate
cortex and dorsomedial prefrontal cortex, as well as indirectly
via projections from the central nucleus of the amygdala and the
hypothalamus (see Counts and Mufson, 2012). The locus coeruleus
also receives ascending interoceptive and nociceptive prediction
errors (see Counts and Mufson, 2012). This is yet another way that
allostasis is altered by modulating the gain or excitability of neurons
that represent sensory and motor prediction errors.
18 In a fly brain, the mushroom bodies may play an analogous role in
predictive coding (Sterling and Laughlin, 2015)
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have refined these hypotheses (see Figure 6). I hypothesize, as
others do (Mesulam, 2002; Hassabis and Maguire, 2009; Buckner,
2012), that the default mode network is necessary for the brain’s
internal model. Regardless of the other mental categories
mapped to default mode network activity, the simulations initiated
within this network cascade to create concepts that eventually
categorize sensory inputs and guide movements in the
service of allostasis. This hypothesis is partially consistent with
the hypothesis that the default mode network represents semantic
concepts (Binder et al., 2009; Binder and Desai, 2011) (see
Figure 4B). I hypothesize that the default mode network hosts
‘part’ of their patterns, but simulations are more than just
multimodal sensorimotor summaries; they are fully embodied
brain states. They emerge as default mode summaries cascade
out to primary sensory and motor regions to become detailed
and particularized [i.e. to modulate the spiking patterns of sensory
and motor neurons (Barrett, 2017); for supporting evidence
on embodied representations of concepts, see (Pulvermu¨ ller,
2013; Fernandino et al., 2015, 2016; Barsalou, 2016).19
I further hypothesize that the salience network tunes the internal
model by predicting which prediction errors to pay attention
to [i.e. those errors that are likely to be allostatically
relevant and therefore worth the cost of encoding and consolidation;
called precision signals (Feldman and Friston, 2010;
Clark, 2013a,b; Moran et al., 2013; Shipp et al., 2013)].20
Specifically, I hypothesize that precision signals optimize the
sampling of the sensory periphery for allostasis, and they are
sent to every sensory system in the brain (for anatomical and
functional justifications, see (Chanes and Barrett, 2016)]. They
directly alter the gain on neurons that compute prediction error
from incoming sensory input (i.e. they apply attention) to signal
the degree of confidence in the predictions (i.e. the priors), confidence
in the reliability or quality of incoming sensory signals,
and/or predicted relevance for allostasis. Unexpected sensory
inputs that are anticipated to have resource implications (i.e.
are likely to impact survival, offering reward or threat, or are of
uncertain value) will be treated as ‘signal’ and learned (i.e.
encoded) to better predict energy needs in the future, with all
other prediction error treated as ‘noise’ and safely ignored (Li
and McNally, 2014; for discussion, see Barrett, 2017). Limbic regions
within the salience network may also indirectly signal the
precision of incoming sensory inputs via their modulation of
the reticular nucleus that encircles that thalamus and controls
the sensory input that reaches the cortex via thalamocortical
pathways [for relevant anatomy, see (Zikopoulos and Barbas,
2006, 2012; John et al., 2016)].21
My hypothesis, then, is that cortical
limbic regions within the salience network are at the core
of the brain’s ability to adjust its internal model to the conditions
of the sensory periphery, again in the service of allostasis
(e.g. see Figure 6) This is consistent with the salience network’s
role in attention regulation; e.g. (Power et al., 2011; Touroutoglou
et al., 2012; Ullsperger et al., 2014; Uddin, 2015).
In addition, I hypothesize that neurons with the frontoparietal
control network sculpt and maintain simulations for longer
than the several hundred milliseconds it takes to process imminent
prediction errors), and they may also help to suppress or
inhibit simulations whose priors are very low (because those
priors are influenced not only by the current sensory array, but
also by what the brain predicts for the future). It pays to be flexible,
to be able to construct and use patterns that extend over
longer periods of time (different animals have different timescales
that are relevant to their behavioral repertoire and ecological
niche). It’s also valuable to learn on a single trial, without
being guided by recurring statistical regularities in the world,
particularly if you reside in a quickly changing environment. As
a prediction generator, the brain is constructing simulations (as
concepts) across many different timescales (i.e. integrating information
across the few moments that constitute an event, but
also across longer time frames at various scales; for similar
ideas, see Wilson et al., 2010; Hasson et al., 2015). Therefore, a
brain may be pattern matching to categorize not only on short
processing timescales of milliseconds but also on much longer
timescales (seconds to minutes to hours or even longer). The
lesson here, for the science of emotion, is that the brain does
not process individual stimuli—it processes events across temporal
windows. Emotion perception is event perception, not object
perception.22
The theory of constructed emotion
Now we can see how a multi-level, constructionist view like the
theory of constructed emotion offers an approach to understanding
the brain basis of emotion that is consistent with
emerging computational and evolutionary biological views of
the nervous system.23
A brain can be thought of as running an
internal model that controls central pattern generators in the
service of allostasis (for more on pattern generators, see
Burrows, 1996; Sterling and Laughlin, 2015; Swanson, 2000). An
internal model runs on past experiences, implemented as concepts.
A concept is a collection of embodied, whole brain representations
that predict what is about to happen in the sensory
environment, what the best action is to deal with impending
events, and their consequences for allostasis (the latter is made
available to consciousness as affect). Unpredicted information
(i.e. prediction error) is encoded and consolidated whenever it is
predicted to result in a physiological change in state of perceiver
(i.e. whenever it impacts allostasis). Once prediction error is
minimized, a prediction becomes a perception or an experience.
In doing so, the prediction explains the cause of sensory events
and directs action; i.e. it categorizes the sensory event. In this
way, the brain uses past experience to construct a
19 Notice that this hypothesis is species-general: rats have a default
mode network and are not able to engage in mental time travel as far
as we can tell (Hsu et al., 2016), but this in no way disconfirms the hypothesis
that the network is running an internal model of the animal’s
world in the service of allostasis.
20 This allows for the encoding of statistical patterns of uncertain value
that can later be reconstructed when they are of use (Dunsmoor et al.,
2015).
21 Salience regions may also play a role in maintaining the internal
model that is unconstrained by the sensory world (such as when constructing
memories, imaginings, dreams, reveries, mind-wandering
and so on). Salience regions also help accomplish multimodal integration
[compare, e.g. the topography of the salience network and the
multimodal integration network found in Sepulcre et al. (2012)].
22 The frontopartial control network (which contains key limbic rich
club hubs in the midcingulate cortex and anterior insula) may also
have a role to play in managing sensory prediction errors, by applying
attention to select those body movements that will generate the expected
sensory inputs, presumably with help from cerebellar and striatal
prediction errors.
23 The theory of constructed emotion integrates ideas and empirical
findings from neuroconstruction (Mareschal et al., 2007; Westermann
et al., 2007; Karmiloff-Smith, 2009), rational constructivism (Xu and
Kushnir, 2013), psychological construction (Russell, 2003; Barrett,
2006b, 2012, 2013; Barrett et al., 2015) and social construction (Boiger
and Mesquita, 2012), as well as descriptive appraisal theories (e.g.,
Clore and Ortony, 2008).
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categorization [a situated conceptualization; (Barsalou, 1999;
Barsalou et al., 2003; Barrett, 2006b; Barrett et al., 2015)] that best
fits the situation to guide action. The brain continually constructs
concepts and creates categories to identify what the sensory
inputs are, infers a causal explanation for what caused
them, and drives action plans for what to do about them. When
the internal model creates an emotion concept, the eventual
categorization results in an instance of emotion.
This hypothesis is consistent with the conceptual innovations
in Darwin’s On the Origin of Species [(Darwin, 1859/1964),
even as it is inconsistent with ‘The Expression of the Emotions in
Man and Animals’ (Darwin, 1872/2005); for a discussion, see
Barrett, 2017]. Some of the psychological constructs used in the
theory of constructed emotion are species-general (e.g. allostasis,
interoception, affect, and concept), while others require the
capacity for certain types of concepts (Barrett, 2012) and are
more species-specific (e.g. emotion concepts). It is necessary to
understand which constructs are species-general vs. speciesspecific
to solve the puzzle of the biological basis of emotion.
Mistaking one for the other is a category error that interferes
with scientific progress.
Constructionism, as a scientific paradigm, makes different
assumptions than the classical paradigm (Barrett, 2015), asks
different questions, and requires different methods and analytic
procedures than those of the classical view (whose methods are
ill-suited to testing it). As a consequence, constructionism is
often profoundly misunderstood [for two recent examples, see
(Anderson and Adolphs, 2014; Kragel and LaBar, 2016)]. With
these observations in mind, here is a partial list of claims I am
not making, to avoid further confusion:
i. I am not saying that emotions are illusions. I’m saying
that emotion categories don’t have distinct, dedicated
neural essences. Emotion categories are as real as any
other conceptual categories that require a human perceiver
for existence, such as ‘money’ (i.e. the various objects
that have served as currency throughout human
history share no physical similarities; Barrett, 2012, 2017).
ii. I am not saying that all neurons do everything (a.k.a. equipotentiality).
I am suggesting that a given neuron does
more than one thing (has more than one receptive field),
and that there are no emotion-specific neurons.
iii. I am not claiming that networks are Lego blocks with a static
configuration and an essential function. I am suggesting that,
when it comes to understanding the physical basis of psychological
categories, it is necessary to focus on ensembles of
neurons rather than individual neurons. A neuron does not
function on its own, and many neurons are part of more than
one network. Moreover, networks function via degeneracy,
meaning that a given network has a repertoire of functional
configurations (i.e. functional motifs) that is constrained by
its anatomical structure (i.e. its structural motif).
iv. I am not claiming that subcortical regions are irrelevant to
emotion. I hypothesize that an instance of emotion is a brain
state that makes the sensory array meaningful, and in so
doing engages the pattern generators for whatever actions
are functional in the context, given a person’s current state.
v. I am not saying that the default mode and salience networks
implement allostasis and therefore should not be
mapped to other psychological categories. I am claiming
that these (and other) domain-general networks can be
mapped to many psychological categories at the same time.
Fig. 6. A large-scale system for allostasis and interoception in the human brain. (A) The system implementing allostasis and interoception is composed of two large-scale
intrinsic networks (shown in red and blue) that are interconnected by several hubs (shown in purple; for coordinates, see Kleckner et al., in press). Hubs belonging to the
‘rich club’ are labeled. These maps were constructed with resting state BOLD data from 280 participants, binarized at p < 10À5
, and then replicated on a second sample of
270 participants. vaIns, ventral anterior insula; MCC, midcingulate cortex; PHG, parahippocampal gyrus; PostCG, postcentral gyrus; PAG, periaqueductal gray; PBN, parabrachial
nucleus; NTS, the nucleus of the solitary tract; vStriat., ventral striatum; Hypothal, hypothalamus. (B) Reliable subcortical connections, thresholded P < 0.05 uncorrected,
replicated in 270 participants.
L. F. Barrett | 13
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vi. I am not saying that concepts are stored in the default
mode network. I’m saying that the default mode network
represents efficient, multimodal summaries, from which a
cascade of predictions issues through the entire cortical
sheet, terminating in primary sensory and motor regions.
The whole cascade is an instance of a concept.
vii. I am not saying that emotions are deliberate, nor denying
that automaticity exists. I am saying that in humans, actual
executive control (e.g. via the frontoparietal control
network in primates) and the experience of feeling in control
are not synonymous (Barrett et al., 2004). All animal
brains create concepts to categorize sensory inputs and
guide action in an obligatory and automatic way, outside
of awareness. Automaticity and control are different brain
modes (each of which can be achieved with a variety of
network configurations), not two battling brain systems.
viii. I am not saying that non-human animals are emotionless.
I’m saying that emotion is perceiver-dependent, so questions
about the nature of emotion must include a
perceiver. ‘Is the fly fearful?’ is not a scientific question,
but ‘Does a human perceive fear in the fly?’ and ‘Does the
fly feel fear?’ can be answered scientifically (and the answers
are ‘yes’ and ‘no’). Notice that I am not claiming that
a fly feels nothing; it may feel affect (Barrett, 2017).
Selected implications of the theory
Scientific revolutions are difficult. At the beginning, new paradigms
raise more questions than they answer. They may explain
existing anomalies or redefine lingering questions out of
existence, but they also introduce a new set of questions that
can be answered only with new experimental and computational
techniques. This is a feature, not a bug, because it fosters
scientific discovery (Firestein, 2012). A new paradigm barely
gets started before it is criticized for not providing all the answers.
But progress in science is often not answering old questions
but asking better ones. The value of a new approach is
never based on answering the questions of the old approach.
Table 2. Selected neuroscience evidence supporting the theory of constructed emotion
Observation Method Example Citations
Degeneracy: mapping many neurons, regions,
networks or patterns to one emotion category
Human neuroimaging: task-related
data
(Vytal and Hamann, 2010; Lindquist et al.,
2012; Wilson-Mendenhall et al., 2011, 2015;
Oosterwijk et al, 2015)
Degeneracy: mapping many neurons, regions,
networks or patterns to one emotion category
Human neuroimaging: multi-voxel
pattern analysis
(Clark-Polner, Johnson and barrett, 2016);
compare the different patterns for a given
emotion category across (Kragel and LaBar,
2015; Wager et al., 2015; Saarimaki et al.,
2016)
Degeneracy: mapping many neurons, regions,
networks, or patterns to one emotion category
Intracranial stimulation in humans (Guillory and Bujarski, 2014)
Degeneracy: mapping many neurons, regions,
networks, or patterns to one emotion category
Behavioral observations in humans
with amygdala lesions
(Becker et al., 2012; Mihov et al., 2013)
Degeneracy: mapping many neurons, regions,
networks, or patterns to one emotion category
Optogenetic research showing many
to one mappings for behaviors in
rodents
(Herry and Johansen, 2014)
Neural reuse: Mapping one neural assembly to
many emotion categories
Human neuroimaging: task-related
data
(Vytal and Hamann, 2010; WilsonMendenhall
et al., 2011; Lindquist et al.,
2012)
Neural reuse: Mapping one neural assembly to
many emotion categories
Human neuroimaging: intrinsic connectivity
data
(Wilson-Mendenhall et al., 2011; Barrett and
Satpute, 2013; Touroutoglou et al., 2015)
Neural reuse: Mapping one neural assembly to
many emotion categories
Optogenetic research and some lesion
research in rodents
(Tovote et al., 2015)
Predictive coding explains aversive (‘fear’)
learning
Optogenetic research and some lesion
research in rodents
(Furlong et al., 2010; McNally et al., 2011; Li
and McNally, 2014)
Emotion concepts are embodied Human neuroimaging: task-related
data
(Oosterwijk et al., 2012, 2015)
Multimodal summaries of emotion concepts are
represented in the default mode network
Human neuroimaging: task-related
data
(Peelen et al., 2010; Skerry and Saxe, 2015)
Default mode and salience network interconnectivity
is associated with the intensity of emotional
experiences (as distinct from arousal)
Human neuroimaging: task-related
data
(Raz et al., 2016)
Embodied simulations are associated with
increased activity in primary interoceptive
cortex
Human neuroimaging: task-related
data
(Wilson-Mendenhall et al., under review)
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Such is the case with the theory of constructed emotion.
Evidence from various domains of research is consistent with
the proposed hypotheses (for select neuroscience examples, see
Table 2), even as it casts aside some of the old unanswered
questions of the classical view.
Ironically, perhaps the strongest evidence to date for the
theory comes from studies that use pattern classification to distinguish
categories of emotion. Several recent articles taking
this approach have reported success in differentiating one emotion
category from another—a finding that is routinely construed
as providing the long awaited support for the classical
view (Kassam et al., 2013; Kragel and LaBar, 2015; Saarimaki et
al., 2016). However, patterns that distinguish among the categories
in one study do not replicate in the other studies. The same
is true for studies that successfully created different patterns of
autonomic physiology, despite using the same stimuli and experimental
method, and sampling from the same population
(e.g. Stephens et al., 2010; Kragel and LaBar, 2013).
Generally speaking, pattern classification results in the science
of emotion are routinely misinterpreted. A pattern that
diagnoses sadness is not the brain state for sadness but merely
a statistical summary of a highly variable set of instances. To
assume otherwise is an essentialist error that mistakes a statistical
summary for the norm.24
Indeed, the voxels that make up
a pattern for a category need not observed in every (or even any)
single instance of that category. A classic study by Posner and
Keele (1968) demonstrated a similar general phenomenon
almost half a century ago, and we have confirmed this with a
simple mathematical simulation (see Clark-Polner, Johnson and
Barrett, 2016).
The theory of constructed emotion is consistent with the
older literature on decorticate animals that appears to support
the classical view. For example, consider the experiment by
Woodworth and Sherrington (1904), who surgically removed the
cerebral cortex, thalamus, and hypothalamus of cats, and
observed what they referred to as ‘pseud-affective’ (for pseudoaffective)
reflexes—reflexive motor actions were left intact but
the ‘affective’ (i.e. allostatic) driver of these responses was gone.
As a consequence, these animals appeared to behave emotionally,
but the actions were no longer in service of survival. These
findings can be interpreted as demonstrating the existence of
pattern generators when the machinery of the conceptual system
has been removed. A similar observation can be made for
Cannon and Britton’s (1925) ‘sham rage’ where a decorticated
cat, upon waking from anesthesia, spontaneously spit, clawed,
and arched its back. Importantly, Cannon referred to these actions
as ‘fury’ and in doing so, inferred the presence of a mental
state from a set of actions.
Scientists carefully map the circuitry for behaviors (or mere
movements in some cases) in non-human animals, but some
mistakenly believe that they are mapping the circuitry for emotions.
An example is observing freezing behavior in a rat (e.g. in
response to electric shock) and calling it ‘fear’. Rats don’t freeze
only in situations that we perceive as threatening (i.e. one behavior
maps to many categories), and rats exhibit a variety of
behaviors in threatening situations (i.e. many behaviors map to
one category). This error, assuming that an action is equivalent
to an emotion, which I call the mental inference fallacy (Barrett,
Box 1. The curious case of SM
Much of our understanding of the neural basis of fear comes from studying Patient S.M. She has difficulty experiencing fear
in many normative circumstances (e.g. horror movies, haunted houses), but she experiences intense fear during experiments
where she is asked to breathe air with higher concentrations of CO2. She is able to mount a normal skin conductance response
to an unexpectedly loud sound, but her brain seems not to use arousal as a learning cue in mild situations (e.g. standard
‘fear learning’ paradigms) and she therefore has difficulty learning from prior errors (e.g. she does not mount an anticipatory
skin conductance response to aversive stimuli, during the Iowa Gambling Task, and she does not show loss aversion
when gambling). Interestingly, however, there is other evidence that S.M. is capable of what is typically called ‘fear learning’.
S.M. is averse to breaking the law for fear of getting in trouble. She also spontaneously reports feeling worried. She is able
‘learn fear’ in the real world (e.g. she is averse to seeking medical treatment or visiting the dentist because of pain she experienced
on a previous occasions).
S.M.’s impairments in fear perception appear to be clearest in experiments where she is asked to view stereotyped, fear
poses and explicitly categorize them as fearful (although she shows more widespread deficits in explicitly perceiving arousal
in posed faces, and she appears to have no difficulty rapidly processing fear faces outside of consciousness). She can perceive
fear in bodies and voices (as is evidenced by her efforts to help her friend or call the police for others in danger). S.M. can
even perceive fear in posed faces when her attention is directed to the eyes of the stimulus face, consistent with evidence
that some amygdala neurons are particularly sensitivity to the sclera of eyes (the faces that depict stereotyped fear poses
contain widen eyes). By contrast, other patients with Urbach-Wiethe Disease spend a longer time looking at the widened
eyes of stereotyped fear poses and have no difficulty correctly categorizing those faces as fearful.
It should be noted (but rarely is) that S.M.’s brain shows abnormalities that extend beyond the amygdala, including the anterior
entorhinal cortex and ventromedial prefrontal cortex, both of which show dense, reciprocal connections to the amygdala
and very likely play a role in S.M.’s specific behavioral profile. It is also important to note that S.M. has had difficulties
sustaining long-term relationships, including friendships, and is distressed by this. There seems to be one clear exception:
S.M. has been able to maintain a relationship with the scientists she has worked with for almost two decades. S.M. calls
them for support (e.g. when she is worried or afraid, such as when did not want to return for painful medical treatment).
They help her with the details of daily life (financial and otherwise). It would be interesting to examine whether S.M. is aware
of their hypothesis that the amygdala contains the circuitry for fear.
For references, see Table 1, and also Feinstein et al. (2016).
24 The average size of a US family in 2015 was 3.14 persons, but that
does not mean that every family (or even any family) contained 3.14
people.
L. F. Barrett | 15
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2017), has wreaked havoc with the scientific accumulation of
knowledge about emotion (also see Barrett, 2012; LeDoux, 2012).
Motor movements do not provide a direct indication of an internal
state, be it in a rodent, a monkey or a human [e.g. see decades
of research on mental inference processes (Gilbert, 1998)
and opacity of mind (Robbins and Rumsey, 2008)].
When viewed in this light, it is an error to claim that studies
of the human brain using functional magnetic resonance imaging
(fMRI) yield different results than studies of non-human animal
brains with lesions or optogenetics (e.g. Adolphs, 2013). In
reality, all are making physical measurements and mapping
emotion concepts to them, and no set of findings is described
appropriately by classical emotion concepts. For example, in an
attempt to deal with all the variation within the category ‘fear’,
scientists create finer-grained typologies in an attempt to bring
nature under control and make it easier to identify their essences
(e.g. Gross and Canteras, 2012). But this does not avoid
the problem of the mental state fallacy. Furthermore, it makes
no sense to elevate categories for anger, sadness, fear, disgust
and happiness to a common ethological framework for comparing
humans with other animals, when there is ample evidence
from linguistics, anthropology and psychology that these categories
do not offer a robust, universal framework for comparing
humans of different cultures (Russell, 1991; Gendron et al.,
2014a,b, 2015; Wierzbicka, 2014; Crivelli et al., 2016).
Conclusions and future directions
Scientists must abandon essentialism and study emotions in all
their variety. We must not merely focus on the few stereotypes
that have been stipulated based on a very selective reading of
Darwin. We must assume variability to be the norm, rather
than a nuisance to be explained after the fact. It will never be
possible to measure an emotion by merely measuring facial
muscle movements, changes in autonomic nervous system signals,
or neural firing within the periaqueductal gray or the
amygdala. To understand the nature of emotion, we must also
model the brain systems that are necessary for making meaning
of physical changes in the body and in the world.
This article is a mere sketch of a much larger scientific landscape.
The theory of constructed emotion proposes that emotions
should be modeled holistically, as whole brain-body
phenomena in context. My key hypothesis is that the dynamics
of the default mode, salience and frontoparietal control networks
form the computational core of a brain’s dynamic internal
working model of the body in the world, entraining
sensory and motor systems to create multi-sensory representations
of the world at various time scales from the perspective of
someone who has a body, all in the service of allostasis (for evidence
consistent with this view, see van den Heuvel et al., 2012;
van den Heuvel and Sporns, 2011, 2013). In other words, allostasis
(predictively regulating the internal milieu) and interoception
(representing the internal milieu) are at the anatomical and
functional core of the nervous system. These insights offer a
range of new hypotheses—e.g. that reappraisal and other regulation
processes (Etkin et al., 2015; Gross, 2015) are accomplished
with predictions that categorize sensory inputs and control action
with concepts (see Figure 4C).
The theory of constructed emotion also views the distinction
between the central and peripheral nervous systems as historical
rather than as scientifically accurate. For example, ascending
interoceptive signals bring sensory prediction errors from
the internal milieu to the brain via lamina I and vagal afferent
pathways, and they are anatomically positioned to be
modulated by descending visceromotor predictions that control
the internal milieu (e.g. Fields, 2004). This suggests the hypothesis
that concepts (i.e. prediction signals) act like a volume dial
to influence the processing of prediction errors before they even
reach the brain. This provides new hypotheses about the chronification
of pain (see Barrett, 2017) that considers pain and emotion
as two sides of the same coin, rather than separate
phenomena that influence one another.
Emotions are constructions of the world, not reactions to it.
This insight is a game changer for the science of emotion. It dissolves
many of the debates that remained mired in philosophical
confusion, and allows us to better understand the value of
non-human animal models, without resorting to the perils of
essentialism and anthropomorphism. It provides a common
framework for understanding mental, physical, and neurodegenerative
disorders (e.g., Barrett and Simmons, 2015; Barrett,
Quigley & Hamilton, 2016; Barrett, 2017), and collapses the artificial
boundaries between cognitive, affective, and social neurosciences
(see Barrett & Satpute, 2013). Ultimately, the theory of
constructed emotion equips scientists with new conceptual
tools to solve the age-old mysteries of how a human nervous
system creates a human mind.
Funding
This article was prepared with support from the National
Institute on Aging (R01 AG030311), the National Cancer
Institute (U01 CA193632), the National Science Foundation
(CMMI 1638234) and the US Army Research Institute for the
Behavioral and Social Sciences (W911NF-15-1-0647 and
W911NF- 16-1-0191). The views, opinions, and/or findings
contained in this paper are those of the authors and shall
not be construed as an official Department of the Army position,
policy, or decision, unless so designated by other
documents.
Conflict of interest. None declared.
Glossary
Agranular: Cerebral cortex with the least developed laminar organization
involving no definable layer IV, and no clear distinction
between the neurons in layers II and III.
Allostasis: Regulating the internal milieu by anticipating
physiological needs and preparing to meet them before they
arise.
Concept: Traditionally, a category is a group of instances that
are similar for some function or purpose; a concept is the mental
representations of those category members. In the theory of
constructed emotion, a concept is a collection of embodied,
whole brain representations that predicts what is about to happen
in the sensory environment, what the best action is to deal
with these impending events, and their consequences for
allostasis.
Degeneracy: Degeneracy refers to the capacity for biologically
dissimilar systems or processes to give rise to identical functions.
Degeneracy is different from redundancy (which is inefficient
and to be avoided).
Dysgranular: Cerebral cortex with a moderately developed
laminar organization involving a rudimentary layer IV and better
developed layers II and III.
Hub: A group of the brain’s most inter-connected neurons.
The hubs with the most dense connections are referred to as
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‘rich club’ hubs, and include visceromotor regions, as well as
other heteromodal regions. They are thought to function as a
high-capacity backbone for synchronizing neural activity, integrating
information (and segregating noise) across the entire
brain.
Internal Milieu: An integrated sensory representation of the
physiological state of the body.
Laminar Organization: The architectural organization of neurons
in a cortical column.
Naı¨ve Realism: The belief that one’s senses provide an accurate
and objective representation of the world.
Pattern Generators: Groups of neurons (i.e. nuclei) that implement
the sequences of actions for coordinated behaviors like
feeding, running, and mating. An action is a single movement
but a behavior is an event. Pattern generators are in the hypothalamus
and down in the brainstem near their effector
muscles and organs (Sterling and Laughlin, 2015; Swanson,
2005).
Visceromotor: Internal movements involving autonomic, neuroendocrine,
and immune systems
Acknowledgements
We thank to Ajay Satpute, Amitai Shenhav, Suzanne
Oosterwijk and Eliza Bliss-Moreau who read and/or made
invaluable comments on an earlier draft of this article.
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