2003 NaturePublishing Group
H I G H L I G H T S
NATURE REVIEWS | NEUROSCIENCE VOLUME 4 | JULY 2003 | 527
Like bats -- and submarines --
dolphins use echolocation to investi-
gate their environment. Unlike bats
and submarines, though, how dol-
phins use this specialized sensory
system is not well understood. A
study of dolphins in the wild now
reveals that they use a unique gain
control system.
One problem faced by any echo-
locating organism is loss of the signal
over distance.An echo from a distant
prey animal will be much fainter than
an echo from the same animal when
it is very close. Bats overcome this
problem using a system of auditory
gain control -- a specialized muscle
in their middle ear contracts when
they emit an echolocation call,which
reduces the sensitivity of the auditory
system and prevents the animal from
being deafened by the call. Then, as
the time from the call increases, the
muscle relaxes and the ear gradually
becomes more sensitive. The system
is calibrated so that the amplitude of
the echo signal remains constant
regardless of how close the target is,
within a certain range.Sonar systems
engineered by humans use a similar
principle.
Au and Benoit-Bird find that
echolocating dolphins also use gain
control to maintain a consistent
signal -- but rather than adjusting
their receivers, they vary the strength
of their calls with the distance to the
target. The net effect is the same --
the calls are precisely calibrated so
that the returning signal has the same
strength regardless of the range to
the target.
So dolphins and bats, faced with
the same problem in their unusual
sensory system, have evolved two
very different mechanisms that
produce the same outcome. Bats use
a neural mechanism that couples
muscle contraction with the echo-
location call; however, it seems that
the dolphin's gain control is a
natural result of their system of
sound production.As they get closer
to a target and the echoes are
returned more rapidly, dolphins
produce echolocation clicks more
quickly; and because of the way the
clicks are produced (which relies on
pressurization of the nasal system)
the amplitude of the clicks will
naturally fall as the repetition rate
increases. What at first seems like a
physiological limitation has been
turned into an efficient gain control
system.
Rachel Jones
References and links
ORIGINAL RESEARCH PAPER Au, W. W. L. &
Benoit-Bird, K. J. Automatic gain control in the
echolocation system of dolphins. Nature 423,
861­863 (2003)
Dolphins turn down
the volume
S E N SO RY SYSTE MS
IN BRIEF
Filopodial calcium transients regulate growth cone
motility and guidance through local activation of calpain.
Robles, E. et al. Neuron 38, 597­609 (2003)
Calcium transients in filopodia affect growth cone motility, but
their downstream effectors are unknown. Here, the authors show
that calpain is one of these effectors; it promotes a decrease in
tyrosine dephosphorylation, the net effect of which is filopodial
stabilization, reduced outgrowth and repulsive turning.
Action potentials in basal and oblique dendrites of rat
neocortical pyramidal neurons.
Antic, S. D. J. Physiol. (Lond.) 9 May 2003 (doi:10.1113/jphysiol.2002.033746)
The apical dendrites of pyramidal cells markedly modulate
backpropagating action potentials,owing to the existence of active
conductances.By using voltage-sensitive dyes,the author found
this not to be the case for basal and oblique dendrites,which
behaved as an integral part of the axosomatic compartment.
NompC TRP channel required for vertebrate sensory
hair cell mechanotransduction
Sidi, S. et al. Science. 12 June 2003 (doi:10.1126/science.1084370))
The mechanosensitive channel that mediates the excitation of hair
cells in the inner ear in response to sound is unknown. Here, the
authors identify the zebrafish homologue of the Drosophila
protein NompC as the missing channel. Reducing NompC
expression in zebrafish embryos led to a reduction of electrical
responses in hair cells, deafness and loss of balance.
Agonist unbinding from receptor dictates the nature of
deactivation kinetics of G protein-gated K+
channels.
Benians, A. et al. Proc. Natl Acad. Sci. USA 100, 6239­6244 (2003)
G protein-gated K+
channels are activated as a result of agoinst
binding to G-protein-coupled receptors (GPCRs), and their
deactivation depends on the hydrolysis of GTP by G after
agonist removal. Here, the authors identify a new deactivation
mechanism; for some agonists, the rate of unbinding from the
GPCR is the key step in the termination of channel activity.
Neurons but not glial cells show reciprocal imprinting of
sense and antisense transcripts of Ube3a.
Yamasaki, K. et al. Hum. Mol. Genet. 12, 837­847 (2003)
The authors report that the mouse Ube3a gene, which codes for a
ubiquitin ligase, is transcribed from both alleles in glia, but only
from the maternal allele in neurons. This is the first evidence that
genomic imprinting is cell-type specific in the brain.
N E U ROG E N ETICS
ION CHA N N E LS
S E N SO RY SYSTE MS
N E U ROPHYS IOLOGY
PROCE SS OUTG ROWTH
Image courtesy of Andre Seale, University of Hawaii.