Susumu Tomita, PhD

Associate Professor of Cellular and Molecular Physiology

Research Organizations

Cellular & Molecular Physiology

Interdepartmental Neuroscience Program

Kavli Institute for Neuroscience

Program in Cellular Neuroscience, Neurodegeneration and Repair

Research Summary

My laboratory's approach to understand the brain is to reduce the brain to various components and ultimately molecules. Temporally, neurotransmission by a major excitatory neurotransmitter, glutamate, is very quick and is clearly essential for brain function; however, the modulation of brain function underlying learning,
memory, emotion, cognition, etc., happens on a different time scale than that of neurotransmission. Our broad goal is to understand how basic synaptic
transmission can be modulated over seconds to hours, thereby supporting complex brain functions. The efficacy of synaptic transmission is determined
by glutamate concentration at the synaptic cleft and by the number and channel properties of the glutamate receptors, which can be modulated by neuronal activation (synaptic plasticity). We have uncovered a network of modulatory proteins for glutamate receptors to control their number and properties. By understanding the machinery that controls the number and channel properties of
glutamate receptors, we hope to reveal the principal rules governing synaptic transmission and synaptic plasticity.

Extensive Research Description

My laboratory’s approach to understand brain is to reduce brain to various components and ultimately molecules. The primary functional component of brain is the neural circuit, which are comprised of anatomical neuronal wiring and synaptic transmission. Temporally, neurotransmission by a major excitatory neurotransmitter in brain, glutamate, is very quick and is clearly essential for brain function; however, the modulation of brain function underlying learning, memory, emotion, cognition, etc., happens on a different time scale than that of neurotransmission. Our broad goal is to understand how basic synaptic transmission can be modulated over seconds to hours, thereby supporting complex brain functions.The efficacy of synaptic transmission is determined by glutamate concentration at the synaptic cleft and by the number and channel properties of the glutamate receptors, which can be modulated by neuronal activation (synaptic plasticity).

It is therefore important to determine how many receptors are at synapses and how strongly these receptors are activated upon glutamate releases. We have uncovered a network of modulatory proteins for glutamate receptors to control their number and properties. By understanding the machinery that controls the number and channel properties of glutamate receptors, we hope to reveal the principal rules governing synaptic transmission and synaptic plasticity. Combined with neuronal wiring mapping, this should help us understand a big picture of neural circuits and the momentary changes that occur in neural circuits to control animal behavior.

Selected Publications

Edit this profile

Contact Info

Susumu Tomita, PhD
Mailing Address
Department of Cellular & Molecular PhysiologyPO Box 208026
333 Cedar Street

New Haven, CT 06520-8026

Tomita Lab.

Research Image 2

A, TARPs consist of four isoforms (stargazin, g -3, g -4, and g -8), which show distinct expression patterns in the brain . B, TARPs (green) colocalize with the glutamatergic markers AMPA receptors (red)(left panel), but not with the GABAergic marker GAD65 (red)(right panel). C, TARPs both modulate trafficking of AMPA receptors to the synapses and control the gating and pharmacology of the channel. Oocytes injected with GluR1 alone are more sensitive to glutamate (Glu) than to kainate (KA). D, AMPA receptor subunits GluR1, GluR2 and GluR4 co-immunoprecipitate with stargazin (STG) in brain extracts from +/stg mice (+/-), but not in extracts from stg/stg mice (-/-). E, TARPs stabilize AMPA receptors at synapses through its C-terminal PDZ domain binding motif.