Identification of the gene that defines a variety of the strength of plasticity in mouse primary visual cortex

2021 Fiscal Year Final Research Report

• Project/Area Number: 18K06476
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 46010:Neuroscience-general-related
• Research Institution: National Institute for Physiological Sciences
• Principal Investigator: Hayashi Kenji 生理学研究所, 基盤神経科学研究領域, 助教 (50512349)
• Project Period (FY): 2018-04-01 – 2022-03-31
• Keywords: 一酸化窒素

Outline of Final Research Achievements

Nitric oxide (NO) is known to be a diffuse mediator for modifying the efficacy of synaptic transmission. In the cortex, NO relates to long-term plasticity by affecting neighboring cells, but the in vivo cortical function is elusive.
Here we show that cortical NO inhibits ocular dominance plasticity. We developed an AAV-DREADD based on Tet-system to specifically and sufficiently activate nitric oxide synthase 1 (NOS1) positive inhibitory cells in NOS1-IRES-Cre mice. We found that the chronic activation of NOS1+ cells eliminates the ocular dominance shift in monocularly deprived animals with NO-dependent manner. Diffusive NO can act synchronously on the plasticity of the surrounding cell population. Together, NO might play a crucial role as a pacemaker in orhestrate the development of the cell ensemble in visual cortex through reducing the instability.

Free Research Field

神経科学

Academic Significance and Societal Importance of the Research Achievements

我々の研究によりin vivo大脳皮質でNOは可塑性に対して抑制的に働くことが分かってきた。眼優位可塑性の中でも制動の分子メカニズムはほぼ未解明であり、本研究の進展は眼優位可塑性の全体像の理解のための重要な知見となると考えている。