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Nicotinic regulation of sensory information processing in primary auditory cortex

Research Project

Project/Area Number 26430025
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurophysiology / General neuroscience
Research InstitutionSoka University

Principal Investigator

Kawai Hideki  創価大学, 理工学部, 准教授 (90546243)

Co-Investigator(Kenkyū-buntansha) 根本 正史  創価大学, 公私立大学の部局等, その他 (80370980)
Research Collaborator YAMASAKI Kenichi  
INAKUMA Kiyonobu  
NAGAYAMA Takahiro  
SUZUKI Anna  
Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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 / 感覚障害 / 神経伝達 / 聴覚 / ニコチン / ムスカリン / 酵素 / 興奮性シナプス / 転写因子 / S/N比 / 神経情報処理 / 大脳皮質 / シグナル・ノイズ比 / 注意力 / 長期増強
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.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report
  • Research Products

    (3 results)

All 2016 2015 Other

All Int'l Joint Research (1 results) Presentation (2 results) (of which Int'l Joint Research: 1 results)

  • [Int'l Joint Research] University of California, Irvine(米国)

    • Related Report
      2016 Annual Research Report
  • [Presentation] Nicotinic activation of protein kinase A modulates excitatory synapses in pyramidal neurons to regulate sound-evoked responses in the thalamocortical input layers of mouse auditory cortex.2016

    • Author(s)
      Takahiro NAGAYAMA, Kenichi YAMASAKI, Kiyonobu INAKUMA, and Hideki D. KAWAI
    • Organizer
      Society for Neuroscience
    • Place of Presentation
      San Diego, California, USA
    • Related Report
      2016 Annual Research Report
    • Int'l Joint Research
  • [Presentation] Nicotinic enhancement of sound-evoked responses in auditory cortex involves phosporylation of extracellular signal-regulated kinases and GluA1 subunit of AMPA receptors.2015

    • Author(s)
      Kenichi YAMASAKI, Kiyonobu INAKUMA, Takahiro NAGAYAMA, and Hideki D. KAWAI
    • Organizer
      Association for Research in Otolaryngology, 38th Annual Mid-Winter Meeting.
    • Place of Presentation
      Baltimore Marriott Waterfront
    • Year and Date
      2015-02-21
    • Related Report
      2014 Research-status Report

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Published: 2014-04-04   Modified: 2022-02-16  

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