| Project/Area Number |
12680794
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
神経・脳内生理学
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| Research Institution | Osaka University |
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Principal Investigator |
KIMURA Fumitaka Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (00202044)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥3,300,000 (Direct Cost: ¥3,300,000)
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| Keywords | NICOTINIC RECEPTOR / THALAMOCORTICAL SLICE / MUSCARINIC RECEPTOR / OPTICAL RECORDING / BARREL CORTEX / MOUCE / INPUT DEPENDENCE / 視床一皮質切片標本 / ACh / ムスカリニック / ニコチニック / 皮質内由来入力 / 視床由来入力 |
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| Research Abstract |
Wide innervation of cholinergic projections throughout the cortex implies that acetylcholine (ACh) plays an essential role in information processing, but how it works is still enigmatic.
Experimental as well as theoretical work in the olfactory cortex and hippocampus suggests that ACh, via the muscarinic receptors serves to shift the dynamics of the cortical networks into a state where afferent influence predominates over intracortical influence. Recent experiments suggest that nicotinic receptors could also be incorporated in the same context in regulating the cortical functions.
To better understand the role of ACh in the cortex, nicotinic effects on thalamo-cortical transmission were studied in the mouse barrel cortex in response to thalamic stimulation using thalamocortical slices from mice. Nicotine, (1-10 mM, through bath) application enhanced field potentials recorded from layer IV (125.7 + 44.8 % of control, n=8).
Voltage-clamp recordings demonstrated that nicotine reduced the failure rate of EPSCs from layer IV cells, which suggested nicotine enhanced the transmitter release. Optical recording indicated that nicotine not only enhanced excitation across the layers but also recruited a late inhibition (> 150 ms), which was specific to barrel hollow area in layer IV.
This results further substantiate the role of nicotine in facilitating thalamic inputs in the cerebral cortex.
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