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突触前抑制以及GABA(B)受体在多刺艾氏蟹神经肌肉接头处的参与情况。

Presynaptic inhibition and the participation of GABA(B) receptors at neuromuscular junctions of the crab Eriphia spinifrons.

作者信息

Rathmayer W, Djokaj S

机构信息

Department of Biology, University of Konstanz, Germany.

出版信息

J Comp Physiol A. 2000 Mar;186(3):287-98. doi: 10.1007/s003590050429.

DOI:10.1007/s003590050429
PMID:10757244
Abstract

Presynaptic inhibition exerted by the common inhibitor on the closer and opener muscles and by the specific inhibitor on the opener muscle was investigated in the crab Eriphia spinifrons. In the closer muscle, activation of GABA(B) receptors by baclofen reduced the mean quantal content of excitatory junctional currents by about 25%. Blocking GABA(B) receptors with CGP 55845 diminished presynaptic inhibition at a similar percentage. GABA(B) receptor-mediated presynaptic inhibition is linked to G proteins. Application of pertussis toxin eliminated about 25% of the inhibition exerted by the common inhibitory neuron. GABA(B) receptors participate in presynaptic inhibition at release boutons of the slow and the fast closer excitor at a similar percentage. In the opener muscle, presynaptic inhibition of transmitter release from the same endings of the opener excitor was about 15% stronger with the specific inhibitor than with the common inhibitor. About 10% of the presynaptic inhibition produced by either one of the two inhibitors could be abolished by blocking GABA(B) receptors. The amplitudes of the excitatory junctional currents in the opener were reduced in the presence of baclofen by about 25%, suggesting that synaptic terminals of the opener excitor are endowed with a similar percentage of GABA(B) receptors as terminals of the slow and the fast closer excitors. Baclofen had no effect on postsynaptic inhibition, indicating that GABA(B) receptors are not involved in postsynaptic neuromuscular inhibition.

摘要

在多刺艾氏蟹中研究了共同抑制剂对闭合肌和张开肌以及特异性抑制剂对张开肌施加的突触前抑制。在闭合肌中,巴氯芬激活GABA(B)受体可使兴奋性突触后电流的平均量子含量降低约25%。用CGP 55845阻断GABA(B)受体可使突触前抑制以相似的百分比减弱。GABA(B)受体介导的突触前抑制与G蛋白有关。应用百日咳毒素可消除约25%由共同抑制性神经元施加的抑制。GABA(B)受体以相似的百分比参与慢闭合肌兴奋神经元和快闭合肌兴奋神经元释放 boutons处的突触前抑制。在张开肌中,特异性抑制剂对张开肌兴奋神经元相同终末的递质释放的突触前抑制比共同抑制剂强约15%。两种抑制剂中任何一种产生的突触前抑制的约10%可通过阻断GABA(B)受体而消除。在巴氯芬存在的情况下,张开肌中兴奋性突触后电流的幅度降低约25%,这表明张开肌兴奋神经元的突触终末与慢闭合肌兴奋神经元和快闭合肌兴奋神经元的终末具有相似百分比的GABA(B)受体。巴氯芬对突触后抑制无影响,表明GABA(B)受体不参与突触后神经肌肉抑制。

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