Bloom F E
Am J Psychiatry. 1977 Jun;134(6):669-72. doi: 10.1176/ajp.134.6.669.
Current experimental paradigms emphasize neurotransmitter-specific interactions to explain the behavioral effects of benzodiazepines. According to this approach the broad range of effects observed suggests the involvement of several transmitter systems without rigorously establishing that any single transmitter system or physiological synaptic function is either necessary or sufficient to express all benzodiazepine actions. Among the effects that occur, potentiation of amino acid-mediated presynaptic inhibition in the spinal cord and postsynaptic inhibitions elsewhere in the brain are attractive testable hypotheses. However, direct physiological evidence that benzodiazepines stimulate gamma-aminobutyric acid (GABA) or other amino acids specifically and exclusively is needed to corroborate this view.
当前的实验范式强调神经递质特异性相互作用来解释苯二氮䓬类药物的行为效应。根据这种方法，所观察到的广泛效应表明涉及多个递质系统，但并未严格确定任何单一递质系统或生理突触功能对于表达所有苯二氮䓬类药物的作用是必要的或充分的。在已出现的效应中，脊髓中氨基酸介导的突触前抑制增强以及大脑其他部位的突触后抑制是有吸引力的可检验假设。然而，需要直接的生理学证据来证实苯二氮䓬类药物特异性且排他性地刺激γ-氨基丁酸（GABA）或其他氨基酸这一观点。
