Modulatory inputs to trigeminal motoneurons in rat slice preparation

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Intracellular recordings were obtained from rat jaw-closing motoneurons (JCMINs) in slice preparations to investigate the effects of serotonin (5-HT) on the post-spike medium-duration afterhyperpolarization (mAHP) and an involvement of protein kinases in the effects.Application of 50 muM 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 muM).On the other hand, when the mAHP amplitude was increased by raising [Ca ^<2+1>]。 from 2 to 6 mM, 5-HT-induced attenuation of the mAHP amplitude was enhanced and even 50 muM 5-HT reduced the mAHP amplitude.This 5-HT-induced suppression of the mAHP could be mimicked by application of membrane-permeable cAMP analog 8-Br- 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 muM 5-HT under raised [Ca ^<2+>]。 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 almost completely blocked by H89, suggesting that the PKC action on the mAHP requires PKA activation.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+>]。We also examied alteration of intracellular calcium concentration ([Ca^<2+>]). [Ca^<2+>] increased when burst firing was eliced by current injection.It is suggested that [Ca^<2+>] changes according to motoneuronal activity.