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兴奋性氨基酸及其拮抗剂对猫尾状核神经元膜电位和动作电位的影响。

Effects of excitatory amino acids and their antagonists on membrane and action potentials of cat caudate neurones.

作者信息

Herrling P L, Morris R, Salt T E

出版信息

J Physiol. 1983 Jun;339:207-22. doi: 10.1113/jphysiol.1983.sp014712.

Abstract

The electrical activity of caudate neurones was recorded with intracellular electrodes in halothane anaesthetized cats. Agonists and antagonists of excitatory amino acid receptors were applied by micro-ionophoresis and their effects on membrane- and action potentials and on cortically evoked synaptic potentials evaluated. The agonists, L-aspartate (asp), L-glutamate (glu), N-methyl-DL-aspartate (NMA), quinolinate and quisqualate all depolarized the membrane, caused repetitive firing, reduced the apparent amplitude of the cortically evoked excitatory post-synaptic potentials (e.p.s.p.s) and increased the amplitude of the associated inhibitory post-synaptic potential. Two of the agonists, NMA and quinolinate, additionally caused the appearance of up to 500 ms long depolarizations (plateaus) on the falling phase of action potentials. These plateaus were seen in about two-thirds of the cells in this sample while in the other third the excitatory effects of NMA and quinolinate were indistinguishable from those of glu and quisqualate. The N-methyl-D-aspartate (NMDA) receptor antagonist D-alpha-aminoadipate (DAA) reversibly inhibited the effects of NMA and quinolinate but only on those cells where these two agents evoked action potential plateaus while on the same cells the effects of asp, glu and quisqualate were either only weakly antagonized or not affected. On cells not displaying plateaus to NMA or quinolinate none of the effects of the agonists could be antagonized by DAA. DAA applications that completely antagonized the effects of NMA never reduced the amplitudes of cortically evoked e.p.s.p.s. Cis-2,3-piperidine dicarboxylate also blocked the effects of NMA and asp at low application currents while at higher currents it enhanced the effects of glu or asp although still retaining its NMA antagonistic activity. High-frequency stimulation of the cortico-caudate pathway resulted in long-lasting depolarizations and repetitive firing, but plateaus of the type caused by NMA or quinolinate were not seen.

摘要

在氟烷麻醉的猫中,用细胞内电极记录尾状核神经元的电活动。通过微离子电泳施加兴奋性氨基酸受体的激动剂和拮抗剂,并评估它们对膜电位、动作电位以及皮质诱发的突触电位的影响。激动剂L-天冬氨酸(asp)、L-谷氨酸(glu)、N-甲基-DL-天冬氨酸(NMA)、喹啉酸和quisqualate均使膜去极化,引起重复放电,降低皮质诱发的兴奋性突触后电位(e.p.s.p.s)的表观幅度,并增加相关抑制性突触后电位的幅度。两种激动剂NMA和喹啉酸,还会在动作电位的下降阶段引起长达500毫秒的去极化(平台期)。在该样本中约三分之二的细胞中可见这些平台期,而在另外三分之一的细胞中,NMA和喹啉酸的兴奋作用与glu和quisqualate的作用无明显差异。N-甲基-D-天冬氨酸(NMDA)受体拮抗剂D-α-氨基己二酸(DAA)可逆性抑制NMA和喹啉酸的作用,但仅对这两种药物诱发动作电位平台期的细胞有效,而在相同细胞上,asp、glu和quisqualate的作用要么仅被微弱拮抗,要么不受影响。在对NMA或喹啉酸不显示平台期的细胞上,DAA不能拮抗激动剂的任何作用。完全拮抗NMA作用的DAA应用从未降低皮质诱发的e.p.s.p.s的幅度。顺式-2,3-哌啶二羧酸在低施加电流时也阻断NMA和asp的作用,而在较高电流时,它增强glu或asp的作用,尽管仍保留其NMA拮抗活性。皮质-尾状核通路的高频刺激导致持久的去极化和重复放电,但未见到由NMA或喹啉酸引起的那种平台期。

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