Cellular and network mechanisms for the oscillatory synchronization between adjacent columns/areas

2017 Fiscal Year Final Research Report

• Project/Area Number: 26290006
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Neurophysiology / General neuroscience
• Research Institution: Kagoshima University (2016-2017); Osaka University (2014-2015)
• Principal Investigator: KANG Youngnam 鹿児島大学, 医歯学総合研究科, 客員研究員 (50177755)
• Co-Investigator(Kenkyū-buntansha): 豊田 博紀 大阪大学, 歯学研究科, 准教授 (00432451) ; 佐藤 元 大阪大学, 歯学研究科, 助教 (10432452) ; 齋藤 充 鹿児島大学, 医歯学域歯学系, 教授 (50347770)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: Insular cortex / CB1 receptor / GPR119 / PPARalpha / Oscillation / Synchronization

Outline of Final Research Achievements

Activation of CB1R by AEA in pyramidal cells in the gustatory insular (Gu-I) cortex caused oscillatory synchronization at theta rhythm, which subsequently propagated into the adjacent gastrointestinal insular (GI-I) cortex. This propagating oscillatory synchronization at theta rhythm was abolished by co-application of GPR119 agonist, and the opposing action between CB1R and GPR119 was found to be mediated by the downregulation and upregulation of cAMP. Prior to the propagation of theta rhythm oscillatory synchronization from Gu-I into GI-I, GABA(B)-mediated feedforward inhibition was caused. A microcut between Gu-I and GI-I revealed the independent oscillations at theta and delta rhythms, respectively, in Gu-I and GI-I, disclosing no feedback from GI-I to Gu-I. These observations suggest that the recognition of umami or sweet taste facilitates the feeding behavior, regardless of hunger or satiety condition.

Free Research Field

神経生理学