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环核苷酸对海兔爆发式起搏器神经元和沉默神经元的作用机制。

Mechanisms of action of cyclic nucleotides on a bursting pacemaker and silent neuron in Aplysia.

作者信息

Drake P F, Treistman S N

出版信息

Brain Res. 1981 Aug 10;218(1-2):243-54. doi: 10.1016/0006-8993(81)91304-4.

Abstract

Cyclic nucleotides are believed to mediate a long-lasting synaptic hyperpolarization in the bursting pacemaker neuron, R15, and are capable of inducing bursting pacemaker activity in the usually silent metacerebral giant cell. Steady state voltage clamp techniques were used to examine the alterations of membrane characteristics produced in these different cell types by cyclic nucleotides. In both cells, IBMX, a phosphodiesterase inhibitor, increased two components: (1) voltage-dependent sodium current and (2) slope conductance believed to reflect potassium flux. The effects of 8-benzylthio-cAMP were identical to those of IBMX in the metacerebral cell. In R15, 8-benzylthio-cAMP affected only the slope conductance. These results are discussed in terms of cyclic nucleotide of bursting pacemaker activity.

摘要

人们认为环核苷酸可介导爆发性起搏神经元R15中持久的突触超极化,并且能够在通常沉默的大脑巨细胞中诱导爆发性起搏活动。运用稳态电压钳技术来检测环核苷酸在这些不同细胞类型中所产生的膜特性变化。在这两种细胞中,磷酸二酯酶抑制剂异丁基甲基黄嘌呤(IBMX)增加了两个成分:(1)电压依赖性钠电流和(2)被认为反映钾通量的斜率电导。在大脑细胞中,8-苄硫基环磷酸腺苷(8-benzylthio-cAMP)的作用与IBMX相同。在R15中,8-苄硫基环磷酸腺苷仅影响斜率电导。本文根据爆发性起搏活动的环核苷酸对这些结果进行了讨论。

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