Nicotinic regulation of sensory information processing in primary auditory cortex

2016 Fiscal Year Final Research Report

• Project/Area Number: 26430025
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: Soka University
• Principal Investigator: Kawai Hideki 創価大学, 理工学部, 准教授 (90546243)
• Research Collaborator: YAMASAKI Kenichi ; INAKUMA Kiyonobu ; NAGAYAMA Takahiro ; SUZUKI Anna
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: ニコチン性受容体 / アセチルコリン / 大脳新皮質 / 聴覚皮質 / 認知症 / 知覚 / 認識

Outline of Final Research Achievements

Systemic nicotine exposure enhances sound evoked responses of specific auditory information while it suppresses those of non-specific information via nicotinic acetylcholine receptors in primary auditory cortex (A1). We investigated mechanisms underlying this nicotinic filtering of sensory information at molecular, cellular, and system levels. Nicotine exposure activated protein kinase A (PKA), which in turn activated extracellular signaling-regulated kinases (ERK) to confer the nicotinic filtering. Nicotine increased the amplitude of spontaneous excitatory synaptic activities via PKA by phosphorylating the subunit of main neurotransmitter glutamate-activated ion channels at or near the synapses. It was also found that nicotine suppressed the responses of inhibitory synaptic activities. These data suggest that nicotinic filtering recruits PKA to regulate both excitatory and inhibitory synapses in A1.

Free Research Field

神経科学