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寄居蟹神经肌肉接头处γ-氨基丁酸介导的抑制作用的电生理研究。

Electrophysiological investigation of GABA-mediated inhibition at the hermit crab neuromuscular junction.

作者信息

Earl J, Large W A

出版信息

J Physiol. 1974 Jan;236(1):113-27. doi: 10.1113/jphysiol.1974.sp010425.

Abstract
  1. The inhibitory neuromuscular junction of the abductor muscle of the large claw of the hermit crab (Eupagurus bernhardus) was investigated using electrophysiological intracellular techniques in order to elucidate further the relative contributions of the pre- and post-synaptic mechanisms of action of GABA and of neural inhibition.2. The electrical constants of the post-synaptic membrane, calculated using the equations for a ;short cable' model, were characteristic of a poorly developed electrical excitability; the specific membrane resistance was usually < 1000 Omega cm(2) and the specific membrane capacitance was > 40 muF/cm(2).3. Stimulation of the excitatory axon to the abductor muscle of the large claw at a frequency of 20 Hz evoked highly facilitating excitatory junction potentials (e.j.p.s); stimulation of the inhibitory axon (60-220 Hz) during the excitatory train elicited inhibition which was manifest as an attenuation of the e.j.p.s.4. The addition of gamma-aminobutyric acid (GABA) to the bathing solution produced a dose-dependent reduction of e.j.p. amplitude and membrane resistance. The inhibitory effect of concentrations (5 x 10(-5) and 1 x 10(-4)M) which caused a 40-75% e.j.p. attenuation could largely be accounted for by a post-synaptic action on membrane conductance.5. Experiments with picrotoxin suggest that presynaptic inhibitory mechanisms have an important role in neurally evoked inhibition.6. Picrotoxin (1-5 x 10(-5)M) effectively blocked neural inhibition and the actions of GABA in this preparation, whereas bicuculline proved to be considerably less potent and therefore less useful as a physiological tool for studying GABA-mediated inhibition in crustacea.
摘要
  1. 为了进一步阐明γ-氨基丁酸(GABA)的突触前和突触后作用机制以及神经抑制的相对贡献,利用电生理细胞内技术对寄居蟹(Eupagurus bernhardus)大爪外展肌的抑制性神经肌肉接头进行了研究。

  2. 根据“短电缆”模型方程计算得出的突触后膜电学常数,具有电兴奋性发育不良的特征;比膜电阻通常<1000Ω·cm²,比膜电容>40μF/cm²。

  3. 以20Hz的频率刺激大爪外展肌的兴奋性轴突,可诱发高度易化的兴奋性接头电位(e.j.p.s);在兴奋性刺激串期间刺激抑制性轴突(60 - 220Hz),可引发抑制,表现为e.j.p.s的衰减。

  4. 向浴液中添加γ-氨基丁酸(GABA)会使e.j.p.幅度和膜电阻呈剂量依赖性降低。浓度为(5×10⁻⁵和1×10⁻⁴M)时,可使e.j.p.衰减40 - 75%,其抑制作用主要可归因于对膜电导的突触后作用。

  5. 用印防己毒素进行的实验表明,突触前抑制机制在神经诱发的抑制中起重要作用。

  6. 印防己毒素(1 - 5×10⁻⁵M)可有效阻断该制剂中的神经抑制和GABA的作用,而荷包牡丹碱的效力明显较低,因此作为研究甲壳类动物中GABA介导的抑制的生理工具不太有用。

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