Dan Feldman
e-mail: dfeldman@ucsd.edu |
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My laboratory is interested in how
circuits in the cerebral cortex process and store information about
the sensory environment. We focus on primary somatosensory (S1) cortex
of the rat, which contains an orderly map of sensory input from the
facial whiskers. The whisker map, like other sensory maps in the
brain, is not fixed, but varies strongly with recent sensory experience.
This phenomenon, called experience-dependent map plasticity,
acts during development to transform immature circuits into appropriately
organized connections that mediate adult sensory perception and sensory-guided
behavior. In adults, such plasticity persists, and is thought to
underlie certain forms of learning, and to contribute to recovery
of function after stroke or peripheral injury. Though map plasticity
occurs with common features across many brain regions, the cellular
and synaptic mechanisms of map plasticity are largely unknown. A
major focus of the lab’s work is to identify these mechanisms,
and to understand how they drive information storage and optimization
of cortical circuits. We are also interested in how S1 encodes and
processes somatosensory input, and how plasticity and learning alter
this processing.
Specific research topics:
Synaptic Mechanisms for Cortical Map Plasticity. Recent evidence suggests that long-term depression (LTD) at specific S1 synapses underlies a major component of whisker map plasticity, the activity-dependent loss of responses to deprived or underused inputs. We are currently testing this hypothesis by studying how sensory deprivation weakens S1 synapses, measured ex vivo in S1 slices from normal and whisker-deprived rats, and by testing whether novel pharmacological and genetic manipulations that selectively block LTD impair map plasticity in vivo. We are also attempting to identify additional sites and mechanisms of map plasticity, including long-term potentiation (LTP), alterations in S1 inhibitory circuirts, and anatomical changes in cortical microcircuits.
Mechanisms and Function of Spike Timing-Dependent Synaptic Plasticity.
How experience induces LTP or LTD in vivo is unknown, and is central
to theories of cortical plasticity. A major effort in the lab is
to test an emerging model that millisecond-scale changes in the timing
of presynaptic and postsynaptic spikes are the key induction signal
for LTP and LTD in S1 in vivo. Such spike timing-dependent
plasticity (STDP) is robust in S1 in vitro, and we showed recently that whisker
deprivation acutely alters the timing of S1 spikes in vivo in a manner
appropriate to drive LTD at relevant S1 synapses. We are now investigating
how different patterns of whisker input generate different spike
timing statistics at S1 synapses, thus leading to different forms
of cortical plasticity. In other experiments, we are examining the
detailed cellular mechanisms for STDP using whole-cell recording
techniques in S1 slices from rats and transgenic mice.
Sensory coding in the whisker system. How sensory information is
encoded and processed in the whisker system is little understood,
beyond simple coding of whisker identity. We are performing in
vivo single unit and whole-cell patch clamp recordings to determine how
S1 neurons respond to complex features of whisker stimuli. We are
also studying how S1 neurons encode natural stimuli in awake, behaving
rats.