焦虑是由于过度频繁地募集gabaergy神经元而导致的gabaergy神经传递减少的一种状态:一种神经生理学模型

Joannis N. Nestoros
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引用次数: 8

摘要

1.1. 所有最常用的抗焦虑药物(苯二氮卓类,巴比妥类,乙醇)选择性地增强gaba介导的神经传递。苯二氮卓类药物产生的gaba增强程度与其对苯二氮卓类受体的相对亲和力密切相关。反复刺激大鼠海马反复抑制性GABA能通路导致GABA有效性显著降低;这种“解除抑制”被抗焦虑药物所抵消。提出了一种神经生理学模型,将焦虑概念化为在“消退”或“脱敏”发生之前,以高于gaba能系统所能适应的频率出现的高度警觉的副产品。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Anxiety as a state of diminished gabaergic neurotransmission resulting from too frequent recruitment of gabaergic neurons: A neurophysiological model

  • 1.

    1. All of the most commonly used antianxiety drugs (benzodiazepines, barbiturates, ethanol) selectively enhance GABA-mediated neurotransmission.

  • 2.

    2. The degree of GABA-potentiation produced by benzodiazepines correlates well with their relative affinities for the benzodiazepine receptor.

  • 3.

    3. Repetitive stimulation of the recurrent inhibitory GABAergic pathway in rat hippocampus leads to a remarkable reduction of the effectiveness of GABA; this “disinhibition” is counteracted by antianxiety drugs.

  • 4.

    4. A neurophysiological model is proposed, conceptualizing anxiety as the by-product of hypervigilance occurring in frequencies higher than those that the GABAergic system can accommodate, before “fading” or “desensitization” occurs.

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