Molecular mechanisms underlying the diversity of Gi/o-coupled receptor-mediated presynaptic depression

2016 Fiscal Year Final Research Report

• Project/Area Number: 26430079
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurochemistry/Neuropharmacology
• Research Institution: National Institute for Physiological Sciences
• Principal Investigator: SATAKE Shin'Ichiro 生理学研究所, 基盤神経科学研究領域, 助教 (30360340)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 小脳 / 顆粒細胞 / 分子層介在ニューロン / 興奮性シナプス後電流 / スライスパッチクランプ法 / グルタミン酸輸送体

Outline of Final Research Achievements

Paired pulse activation of rat cerebellar granule cell (GC) ascending axons at short intervals (30-100 ms) causes not only increase in the peak amplitude (PPFamp) of the second EPSC (EPSC2) recorded from molecular layer interneurons (MLIs) but also prolongation of the EPSC2 decay time (PPPdecay) relative to those of the first EPSC. PPFamp is resulted from transient increases in release probability (Pr) and multivesicular release (MVR), whereas PPPdecay is elicited by an increase in MVR and the subsequent pooling of MVR-glutamate among adjacent synapses. Recently, we found that PPPdecay plays a major role in Gi/o-coupled receptor-mediated presynaptic depression in the GC-MLI synapse. In this study, we focused on molecular mechanisms underlying the presynaptic depression. Dynamic modulation of presynaptic MVR and postsynaptic current decay will provide additional complexity in neuronal encoding, processing, and plasticity at the single synapse to reflect circumstances of adjacent cells.

Free Research Field

神経生理学