# Regulation of glutamate receptors by calcium-dependent protein kinases

> **NIH NIH R01** · YALE UNIVERSITY · 2023 · $418,750

## Abstract

Neural circuits and their dynamic alteration control behavior. Neural circuits are
composed of billions of neurons that communicate at synapses via the process of
synaptic transmission, whereby neurotransmitters are released and bind to their
respective receptors. Synaptic transmission can be persistently modified by neuronal
activity in a process termed synaptic plasticity, acting to dynamically modulate animal
behavior. Conversely, dysregulation of synaptic plasticity contributes to various
psychiatric and cognitive disorders including autism, schizophrenia, mental retardation,
and addiction. Therefore, proper synaptic plasticity is crucial for human health. Among
various types of synaptic plasticity, NMDA receptor (NMDAR)-dependent long-term
potentiation (LTP) has been extensively studied. In this form of LTP, NMDAR activation
increases synaptic AMPA receptor (AMPAR) activity through activation of CaMKII that
drives AMPARs from a reserve pool to synapses. Though more than 100 molecules
have been implicated in LTP, the direct cellular machinery remains unclear. Recently,
we identified TARP-8 as a critical CaMKII substrate for LTP. In this propsal, we aim to
reveal the fundamental mechanisms of AMPAR potentiation during synaptic plasticity.
Successful completion of this proposal will provide fundamental mechanistic insights into
LTP and its roles in controlling animal behavior. Considering synaptic plasticity as a
general model to mediate dynamic brain function, elucidating the molecular mechanisms
underlying the control of synaptic plasticity will enable us to identify putative molecular
targets for drugs to alleviate psychiatric and cognitive disorders. Moreover, the
identification of the critical molecules that control synaptic plasticity directly is a chief
neurobiological goal.

## Key facts

- **NIH application ID:** 10596136
- **Project number:** 5R01MH077939-13
- **Recipient organization:** YALE UNIVERSITY
- **Principal Investigator:** Susumu Tomita
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2023
- **Award amount:** $418,750
- **Award type:** 5
- **Project period:** 2008-08-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10596136

## Citation

> US National Institutes of Health, RePORTER application 10596136, Regulation of glutamate receptors by calcium-dependent protein kinases (5R01MH077939-13). Retrieved via AI Analytics 2026-05-21 from https://api.ai-analytics.org/grant/nih/10596136. Licensed CC0.

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