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Molly M Huntsman

Assistant Professor of Pharmacology
Ph.D., University of California,
Irvine, 1995
(202) 687-6295
mh257@georgetown.edu

                                      

          

The role of inhibition in synaptic plasticity

Synaptic plasticity is customarily associated with excitatory neurotransmission in both hebbian and homeostatic mechanisms. The same is true for the plasticity associated with the repositioning of sensory maps in primary sensory cortex. However, there has always been compelling evidence to suggest that inhibitory neurons contribute to experience-dependent plasticity in sensory cortex. For example, inhibitory neurons are both numerous and diverse in sensory cortical areas. They shape sensory evoked receptive field properties of cortical neurons and are sensitive to changes in activity.  In addition, the functional complexity of GABAA receptor mediated inhibitory neurotransmission is equally diverse.  It is often assumed, that through this diversity, exists a specialization of inhibitory function.  Based on this framework, my lab is focused on four questions toward understanding the role of inhibition in synaptic plasticity:   

1) What types of inhibitory neurons contribute to sensory map plasticity?

 2) What is the mechanism by which this plasticity is mediated? For example, what is the biophysical consequence of sensory deprivation and does this implicate homeostatic or hebbian forms of plasticity?

 3) Do deprivation induced biophysical changes in inhibitory neurons affect sensory processing?

 4) How can we use sensory systems to understand plastic changes that occur in mechanisms of disease, such as epilepsy?

 The overall goal of my research is to establish functional roles for specialized inhibitory circuits in synaptic plasticity and sensory processing. In order to accomplish these goals, I use a combined molecular and physiological approach to understand biophysical consequences of sensory deprivation. I employ the whole cell voltage clamp technique to measure GABAA receptor mediated currents in physiologically identified neurons in layer 4 of the primary somatosensory cortex of mice. These studies will reveal new, fundamental roles of intracortical inhibition in synaptic plasticity by cell-type-specific inhibitory circuits and implicate inhibition in non-hebbian mechanisms of plasticity in the re-organization of sensory maps.    

  Functional properties of sensory deprived neurons. A, Schematic of pattern of main facial whiskers in rows   (A,B,C,D,E). B, Sensory deprivation is achieved through selective whisker removal. This is a schematic of our whisker removal pattern. C, slice in recording chamber showing the pattern of barrels that correspond to each facial whisker in A, B. Each whisker on the contralateral face corresponds to a barrel in layer 4. D, Cytochrome oxidase stained section in whisker trimmed animal shown in B. The lighter staining corresponds to decreased activity in barrels that are postsynaptic to sensory pathways aligned with missing whiskers.


Selected Publications: