Opiate alkaloids antagonize postsynaptic glycine and GABA responses: Correlation with convulsant action
Opiate alkaloids antagonize postsynaptic glycine and GABA responses: Correlation with convulsant action
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DOI：
10.1016/0006-8993(82)90038-5
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发表时间：
1982-03
期刊：
影响因子：
2.9
通讯作者：
M. Werz;R. Macdonald
中科院分区：
文献类型：
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作者：
M. Werz;R. Macdonald
应用细胞内记录技术，在原代分离培养的小鼠脊髓神经元上观察阿片类生物碱和阿片肽对神经元自发活动和突触后氨基酸反应的作用。阿片类药物的应用采用灌注法，氨基酸的应用采用离子导入法。阿片类生物碱可拮抗甘氨酸和GABA反应，但不能拮抗谷氨酸反应。由于阿片对甘氨酸和GABA反应的影响不是纳洛酮可逆的，只有微弱的立体特异性，并且不是由阿片肽[d-Ala2]-Met-脑啡酰胺产生的，这些作用不太可能是由阿片受体介导的。阿片抑制甘氨酸抑制作用与诱发脊髓神经元阵发性去极化有关，提示高浓度阿片类生物碱的惊厥作用可能与抑制氨基酸传递的拮抗作用有关。
Opiate alkaloid and opioid peptide actions on spontaneous neuronal activity and postsynaptic amino acid responsiveness were assessed using intracellular recording techniques applied to murine spinal cord neurons in primary dissociated cell culture. Application of opiates was by superfusion and amino acids by iontophoresis. Glycine and GABA but not glutamate responses were antagonized by the opiate alkaloids. Since opiate effects on glycine and GABA responses were not naloxone-reversible, only weakly stereospecific, and not produced by the opioid peptide [d-Ala2]-Met-enkephalinamide, it is unlikely that these effects were mediated by opiate receptors. Opiate depression of glycine inhibition was correlated with the induction of paroxysmal depolarizations in cultured spinal cord neurons, suggesting that antagonism of inhibitory amino acid transmission may underlie the convulsant actions of high concentrations of the opiate alkaloids.