Anorectic factor modulates synaptic transmission in the insular cortex
| Project/Area Number |
24890260
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthodontic/Pediatric dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
TAKEI Hiroki 日本大学, 歯学部, 助教 (50632543)
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| Project Period (FY) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | レプチン / 島皮質 / IPSC / EPSC / 抑制性シナプス後電流 / 興奮性シナプス後電流 |
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| 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.
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Report
(3 results)
Research Products
(4 results)
