Associate Professor (Neuroscience)
Research areas: , Developmental Neuroscience, Cellular and Molecular Neuroscience
My laboratory studies how cerebral cortex encodes and processes sensory information, and how the brain learns and adapts to patterns in the sensory world. We focus on the rodent’s primary somatosensory (S1) cortex, which processes information from the facial whiskers, which serve as active tactile (touch) detectors analogous to human fingertips. We study how the whisker system extracts tactile information from the world, and how this information is encoded and processed by S1 circuits. We also study how S1 neurons and circuits are altered by recent sensory experience in order to store sensory information and optimize S1 processing according to behavioral needs.
Experiments combine synaptic physiology, single-unit recording, multi-site recording, optical imaging, and behavior, both in vivo and in vitro. The goal is to understand cortical information processing and information storage from the synapse to systems levels. Results of these studies will provide essential basic knowledge to understand common disorders of cortical function and plasticity, including epilepsy, autism, Alzheimer’s disease, and learning disability.Current ProjectsSynaptic Mechanisms for Cortical Map Plasticity
. S1 contains an orderly map of input from the facial whiskers. This whisker map, like other sensory maps in the brain, is not fixed, but varies strongly in response to recent sensory experience, a phenomenon termed experience-dependent map plasticity. During development, map plasticity transforms immature circuits into appropriate adult connections that mediate sensory perception. In adults, map plasticity allows the brain to dynamically allocate processing capacity in response to changing behavioral needs, and is thought to mediate certain forms of sensory learning. We are working to identify the cellular and synaptic mechanisms that drive map plasticity, and to understand how they drive information storage. In one major focus, we are testing whether long-term synaptic depression (LTD) is the mechanism responsible for a major component of map plasticity, the activity-dependent loss of responses to underused sensory inputs. We are also identifying additional mechanisms for map plasticity, including long-term potentiation (LTP), alterations in cortical inhibitory circuits, and anatomical changes in cortical microcircuits.Mechanisms and Function of Spike Timing-Dependent Synaptic Plasticity
. A central tenet of cortical plasticity is that sensory experience can increase or decrease the strength of specific cortical synapses. How this happens is not clear. 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 long-term synaptic potentiation (LTP) and depression (LTD) in vivo. Such spike timing-dependent plasticity (STDP) is robust in S1 in vitro and in vivo, 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.Active sensory coding in the whisker system
. A major feature of sensory systems is that sensory detectors are actively moved to sample the environment (e.g., whiskers, fingertips, eyes, sniffing in the olfactory system). How the brain processes active sensory inputs is not understood. Rats actively sweep their whiskers at 5-12 Hz to detect objects and determine object location, surface features, and shape. We are currently performing several types of experiments to determine how tactile information is extracted by moving whiskers and processed and encoded in somatosensory areas of the cortex. These include multi-site, single-unit recordings during active palpation onto objects, and single-unit and whole-cell patch clamp recordings to determine how S1 neurons encode complex, natural whisker inputs.
Drew PJ, Feldman DE (2007). Representation of moving wavefronts of whisker deflection in rat somatosensory cortex. J. Neurophysiology, Jun 13 [Epub ahead of print]
Bender V, Bender K, Brasier DJ, Feldman DE (2006). Two coincidence detectors for spike timing-dependent plasticity in somatosensory cortex. Journal of Neuroscience, 26: 4166-77.
Bender K, Allen CB, Feldman DE (2006). Synaptic basis for deprivation-induced synaptic weakening in rat somatosensory cortex. Journal of Neuroscience, 26: 4155-65.
Gabernet L, Jadhav SP, Feldman DE, Carandini M, Scanziani M (2005). Somatosensory integration controlled by dynamic thalamocortical feed-forward inhibition. Neuron 48: 1-13.
Feldman DE, Brecht M (2005). Map plasticity in somatosensory cortex. Science 310: 810-5.
Celikel T, Szostak VA, Feldman DE (2004). Modulation of spike timing by sensory deprivation during induction of cortical map plasticity. Nat. Neurosci. 7: 534-541.
Allen CB, Celikel T, Feldman DE (2003). Long-term depression induced by sensory deprivation during cortical map plasticity in vivo. Nat. Neurosci. 6: 291-299.
Feldman DE (2000). Timing-based LTP and LTD at vertical inputs to layer II/III pyramidal cells in rat barrel cortex. Neuron 27: 45-56.