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首页> 外文期刊>Journal of Neurophysiology >Serotonergic modulation of the hyperpolarizing spike afterpotential in rat jaw-closing motoneurons by PKA and PKC.
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Serotonergic modulation of the hyperpolarizing spike afterpotential in rat jaw-closing motoneurons by PKA and PKC.

机译：PKA和PKC对大鼠下颌闭合运动神经元超极化尖峰后电位的血清素能调节。

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Intracellular recordings were obtained from rat jaw-closing motoneurons (JCMNs) in slice preparations to investigate the effects of serotonin (5-HT) on the postspike medium-duration afterhyperpolarization (mAHP) and an involvement of protein kinases in the effects. Application of 50 microM 5-HT caused membrane depolarization and increased input resistance in the most cells without affecting the mAHP, whereas not only membrane depolarization and an increase in input resistance, but also the suppression of the mAHP amplitude was induced by higher dose of 5-HT (100 or 200 microM). On the other hand, when the mAHP amplitude was increased by raising [Ca(2+)](o) from 2 to 6 mM, 5-HT-induced attenuation of the mAHP amplitude was enhanced, and even 50 microM 5-HT reduced the mAHP amplitude. This 5-HT-induced suppression of the mAHP could be mimicked by application of membrane-permeable cAMP analogue 8-Bromo-cAMP, potentiated by the cAMP-specific phosphodiesterase inhibitor Ro 20-1724 and antagonized by protein kinase A (PKA) inhibitor H89. The enhancement of the mAHP attenuation induced by 50 microM 5-HT under raised [Ca(2+)](o) was blocked by a protein kinase C (PKC) inhibitor chelerythrine, suggesting an involvement of PKC in this enhancement. On the other hand, the attenuation of the mAHP induced by PKC activator phorbol 12-myristate 13-acetate was blocked almost completely by H89, suggesting that the PKC action on the mAHP requires PKA activation. Neither 5-HT(1A) antagonist NAN-190 or 5-HT(4) antagonist SB 203186 blocked 5-HT-induced attenuation of the mAHP. We conclude that 5-HT induces dose-dependent attenuation of the mAHP amplitude through cAMP-dependent activation of PKA and that PKC-dependent PKA activation is also likely to be involved in the enhancement of 5-HT-induced attenuation of the mAHP under raised [Ca(2+)](o). Because the slope of the linear relationship between firing frequency and injected current was increased only when the mAHP amplitude was decreased by 5-HT, it is suggested that the relation between incoming synaptic inputs and firing output in JCMNs varies according to serotonergic effects on JCMNs and calcium-dependent modulation of its effects.
机译：从大鼠颚闭合运动神经元（JCMNs）的切片制品中获得细胞内记录，以研究5-羟色胺（5-HT）对加标后持续时间超极化（mAHP）的影响以及蛋白激酶的参与。 50 microM 5-HT的使用在大多数细胞中引起膜去极化和增加的输入电阻，而不影响mAHP，而更高剂量的5剂量不仅引起膜去极化和输入电阻增加，而且还抑制了mAHP幅度。 -HT（100或200 microM）。另一方面，当通过将[Ca（2 +）]（o）从2 mM增加到6 mM来增加mAHP幅度时，会增强5-HT诱导的mAHP幅度衰减，甚至降低了50 microM 5-HT mAHP振幅。这种5-HT诱导的对mAHP的抑制作用可以通过应用膜可渗透的cAMP类似物8-Bromo-cAMP来模拟，该膜由cAMP特异性磷酸二酯酶抑制剂Ro 20-1724增强，并被蛋白激酶A（PKA）抑制剂H89拮抗。在升高的[Ca（2 +）]（o）下由50 microM 5-HT诱导的mAHP衰减的增强被蛋白激酶C（PKC）抑制剂白屈菜红碱阻止，表明PKC参与了这种增强。另一方面，由PKC活化剂佛波醇12-肉豆蔻酸酯13-乙酸酯诱导的mAHP的衰减几乎完全被H89阻断，表明PKC对mAHP的作用需要PKA活化。 5-HT（1A）拮抗剂NAN-190或5-HT（4）拮抗剂SB 203186均未阻止5-HT诱导的mAHP衰减。我们得出结论，5-HT通过依赖cAMP的PKA激活诱导mAHP幅度的剂量依赖性衰减，而依赖PKC的PKA激活也可能在升高的条件下增强了5-HT诱导的mAHP的衰减[Ca（2 +）]（o）。因为仅当mAHP幅度降低5-HT时，激发频率与注入电流之间的线性关系才增加斜率，所以建议JCMNs中突触输入与激发输出之间的关系根据对JCMNs的血清素能影响而变化。钙依赖性调节其作用。

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