2016 Fiscal Year Final Research Report
The mechanism of inhibitory effect by inhibitory postsynaptic potentials via alpha-2 adrenergic receptor
| Project/Area Number |
25461070
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Showa University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
ONIMARU Hiroshi 昭和大学, 医学部, 客員教授 (30177258)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Keywords | 交感神経 / α2受容体 |
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| Outline of Final Research Achievements |
It is unclear that the excitability of sympathetic preganglionic neurons (SPNs) can be inhibited indirectly (presynaptically). We examined the effects of NE or dexmedetomidine hydrochloride (Dxm) on SPNs by analyzing the excitatory and inhibitory postsynaptic potentials (EPSP, IPSPs) using the whole-cell patch clamp technique in spinal cord slice preparations of rats. EPSPs were dominant in 14 SPNs (EPSP-SPNs) and IPSPs were dominant in 6 SPNs (IPSP-SPNs) at baseline. In cases of 19 SPNs, we couldn’t analyze postsynaptic potentials due to high frequency firings (firing-SPNs). NE gradually depolarized both types of SPNs and NE increased the EPSP frequency of EPSP-SPNsand EPSP voltage of IPSP-SPNs. Dxm inhibited those effects. In some firing-SPNs, NE induced hyperpolarization and inhibited firings. In these neurons, Dxm had no effect. SPNs received inhibitory modulation through α2-adrenergic receptors. Some SPNs can directly be inhibited via effects independent of the α2 receptor.
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| Free Research Field |
内科学 循環器内科学
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