| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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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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