ラット島皮質におけるシナプス前NK1受容体のサブスタンスPによる活性化は一酸化窒素合成を介してEPSCを抑制する

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  • Presynaptic NK1 receptor activation by substance P suppresses EPSCs via nitric oxide synthesis in the rat insular cortex

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<p>Substance P (SP) regulates inhibitory synaptic transmission mediated by GABAA receptors in the cerebral cortex, but the SP-mediated regulation of excitatory synaptic transmission remains poorly understood. We performed whole-cell patch-clamp recordings from pyramidal neurons to examine the effects of SP on EPSCs in the insular cortex (IC), which is involved in nociceptive information processing. We examined EPSCs evoked by minimal electrical stimulation (eEPSCs), including stepwise EPSCs and failure events. The SP-induced suppression of eEPSCs was accompanied by an increase in the paired-pulse ratio and was inhibited by the preapplication of an NK1 receptor antagonist SR140333. [Sar9, Met (O2) 11]-Substance P, NK1 receptor-selective agonists mimicked the effect of SP on eEPSC. Considering that most NK1 receptors are expressed in NOS-positive GABAergic neurons, the SP-induced suppressive effect on EPSCs may be mediated by NO in this subtype of GABAergic neurons. Indeed, SP increased the fluorescence intensity of DAX-J2 Red in some GABAergic neurons. In addition, both L-NAME, an NOS inhibitor, and PTIO, an NO scavenger, diminished the SP-induced suppression of eEPSCs. These results suggest that activation of presynaptic NK1 receptors contributes to SP-induced eEPSC suppression by activating the NO synthesis pathway in GABAergic neurons.</p>

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