Evans R H, Francis A A, Watkins J C
Eur J Pharmacol. 1977 Aug 15;44(4):325-30. doi: 10.1016/0014-2999(77)90306-5.
The effects of some central depressant drugs on amino acid-induced depolarization of motoneurons have been determined in the isolate hemisected frog spinal cord. Motoneuron depolarization was recorded from ventral roots and measurements were made in the presence or absence of procaine or tetrodotoxin to minimize indirect effects of both drugs and amino acids. Chlorpromazine (0.05-0.1 mM) and diazepam (0.5 mM) produced a similar differential pattern of depression of amino acid-induced depolarizations. Responses induced by L-homocysteate were markedly antagonized by these drugs, while responses to quisqualate were unaffected. L-Aspartate-induced responses were antagonized more than L-glutamate-induced responses. This pattern of antagonism resembles that previously described for Mg2+. In contrast, pentobarbital (0.1 or 0.3 mM), and the inhibitory amino acids GABA and beta-alanine (0.5-1.0 mM), depressed amino acid-induced responses in a more uniform manner. The differential effects observed with chlorpromazine and diazepam provide further support for the possibility that responses to excitant amino acids structurally related to L-glutamate may have different underlying mechanisms.
在离体半横断蛙脊髓中,已确定了某些中枢抑制药物对氨基酸诱导的运动神经元去极化的影响。从腹根记录运动神经元的去极化,并在存在或不存在普鲁卡因或河豚毒素的情况下进行测量,以尽量减少药物和氨基酸的间接影响。氯丙嗪(0.05 - 0.1 mM)和地西泮(0.5 mM)对氨基酸诱导的去极化产生了类似的差异性抑制模式。这些药物显著拮抗由L-同型半胱氨酸盐诱导的反应,而对喹啉酸的反应则不受影响。L-天冬氨酸诱导的反应比L-谷氨酸诱导的反应受到的拮抗作用更强。这种拮抗模式类似于先前描述的镁离子的拮抗模式。相比之下,戊巴比妥(0.1或0.3 mM)以及抑制性氨基酸GABA和β-丙氨酸(0.5 - 1.0 mM)以更均匀的方式抑制氨基酸诱导的反应。氯丙嗪和地西泮观察到的差异性效应为以下可能性提供了进一步支持,即对与L-谷氨酸结构相关的兴奋性氨基酸的反应可能具有不同的潜在机制。