2013 Fiscal Year Final Research Report

Anorectic factor modulates synaptic transmission in the insular cortex

Research Project

Project/Area Number	24890260
Research Category	Grant-in-Aid for Research Activity Start-up
Allocation Type	Single-year Grants
Research Field	Orthodontic/Pediatric dentistry
Research Institution	Nihon University
Principal Investigator	TAKEI Hiroki 日本大学, 歯学部, 助教 (50632543)
Project Period (FY)	2012-08-31 – 2014-03-31
Keywords	レプチン / 島皮質
Research Abstract	Leptin and insulin are hormone that suppress appetite. The insular cortex (IC) expresses high density of these receptors. However almost no information is about the functional roles of leptin and insulin in the IC. To explore this, I performed multiple whole-cell patch clamp recording in the IC slice preparation. I found that the amplitude of excitatory postsynaptic current (EPSC) was decreased by leptin. In contrast to EPSC, leptin increased the amplitude of inhibitory postsynaptic current (IPSC) in fast-spiking neuron (FS) to pyramidal cell (Pry) connections via phosphoinositid 3-kinase (PI3-K) and signal transducers and activators of transcription factors 3 (STAT3) cascade. The facilitative effect of leptin on the IPSC were dose dependent. These results suggest leptin is likely to play a role in suppression of gustatory information processing.

(2 results)