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首页> 外文期刊>The European Journal of Neuroscience >Investigation of PKC isoform-specific translocation and targeting of the current of the late afterhyperpolarizing potential of myenteric AH neurons.
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Investigation of PKC isoform-specific translocation and targeting of the current of the late afterhyperpolarizing potential of myenteric AH neurons.

机译：PKC亚型特异性易位和肌间叶AH神经元超极化后后期电流的靶向研究。

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摘要

AH neurons in the enteric nervous system play an essential role in initiating intestinal reflexes and factors that control AH neuron excitability therefore influence the state of the digestive system. Prominent afterhyperpolarizations that follow action potentials in these neurons strongly affect their excitability. In the present work, we have investigated the regulation of the afterhyperpolarizing current (I(AHP)) by protein kinase C (PKC). Electrophysiological responses and protein translocation were investigated in AH neurons of freshly dissected preparations of myenteric ganglia from the guinea-pig ileum. The activator of conventional and novel PKCs, phorbol dibutyrate, but not the activator of novel PKCs, ingenol, blocked the I(AHP). Phorbol dibutyrate had no effect on the hyperpolarization-activated current (I(h)) or on the A current (I(A)). Stimulation of synaptic inputs to the neurons also reduced the I(AHP), and had no effect on I(h) or I(A). Phorbol dibutyrate also reduced a background outward current that was present after the I(AHP) current had been blocked by clotrimazole. Both phorbol dibutyrate and ingenol caused translocation of the novel PKC, PKCepsilon, in these neurons. Only phorbol dibutyrate caused translocation of PKCgamma, a conventional PKC. The studies thus indicate that the activation of PKC by phorbol esters and by nerve stimulation affects AH neurons in a similar way, and that PKC activation targets both the I(AHP) and another background K(+) current. The I(AHP) is targeted by a conventional PKC, suggested to be PKCgamma, as this is the only conventional PKC that is prominent in AH neurons.
机译：肠神经系统中的AH神经元在启动肠道反射中起着至关重要的作用，控制AH神经元兴奋性的因素因此会影响消化系统的状态。在这些神经元中跟随动作电位的明显的超极化后强烈影响其兴奋性。在目前的工作中，我们已经研究了蛋白激酶C（PKC）对超极化后电流（I（AHP））的调节。在豚鼠回肠的肌神经节的新鲜解剖制剂的AH神经元中研究了电生理反应和蛋白质移位。常规和新型PKC的活化剂佛波二丁酸酯，而不是新型PKC的活化剂，丁香酚，阻断了I（AHP）。磷酸佛波酯对超极化激活电流（I（h））或A电流（I（A））没有影响。刺激神经元的突触输入也降低了I（AHP），并且对I（h）或I（A）没有影响。 Phbutol dibutyrate还可以减少本底电流，而I（AHP）电流已被克霉唑阻断。佛波二丁酸酯和丁香酚均引起这些神经元中新型PKC，PKCepsilon的移位。仅佛波醇二丁酸酯引起传统PKCPKCγ的移位。因此，研究表明，佛波酯和神经刺激对PKC的激活以类似的方式影响AH神经元，并且PKC的激活同时针对I（AHP）和另一背景K（+）电流。 I（AHP）被常规PKC靶向，建议是PKCgamma，因为这是在AH神经元中突出的唯一常规PKC。

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