Introduction

Our laboratory studies how the 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 is a major model system for studying cortical function. S1 cortex 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 dynamically 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.

Our goal is to understand basic principles of cortical information processing, information storage and learning, from the synapse to circuit to systems levels. Results from our studies will provide much-needed basic knowledge about brain function, and will enable better understanding of common disorders of cortical function and plasticity, including epilepsy, autism, Alzheimer’s disease, learning disability, and mental retardation.

Areas of current research

Synaptic Mechanisms for Cortical Map Plasticity. A dominant model is that rapid components of cortical map plasticity involve long-term potentiation (LTP) and long-term depression (LTD) at specific cortical synapses. Recent evidence provides the first strong support for this model, but many questions remain. We recently demonstrated that a specific synapse in S1 undergoes LTD during whisker map plasticity. This LTD is likely to underlie a major component of map plasticity, the activity-dependent loss of responses to underused inputs. We are currently testing this hypothesis by studying how whisker trimming weakens S1 synapses, measured using whole-cell recording techniques in brain slices, and by testing whether novel pharmacological and genetic manipulations that selectively block LTD impair map plasticity in vivo. We are also identifying additional sites and mechanisms of map plasticity, including long-term potentiation (LTP), alterations in inhibitory circuits, 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 trimming 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.

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 behavioral analysis of whisker vibrations during whisker use, multi-site tetrode 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.

Time and timing in sensory processing and learning. Precise timing is critical for sensory processing, from speech production and recognition to processing of visual motion, and disruption of rapid temporal processing may be the basic deficit in dyslexia and other language impairment. Recent work from our laboratory indicates that whisker inputs are also encoded with high temporal precision, and that this precision is critical for sensory representation and for plasticity in the cortex. We are currently testing how this temporal precision arises, and its perceptual importance, with the goal of understanding the neurobiological basis for temporal processing deficits, and how they may be remedied. This work is done as part of the National Science Foundation-funded Temporal Dynamics of Learning Center.