Gray J A
Encephale. 1983;9(4 Suppl 2):161B-166B.
From psychopharmacological experiments the concept of a "behavioural inhibition system" (BIS) has been developed. This system responds to novel stimuli or to those associated with punishment or nonreward by inhibiting ongoing behaviour and increasing arousal and attention to the environment. It is activity in the BIS that constitutes anxiety and that is reduced by anti-anxiety drugs (benzodiazepines, barbiturates and alcohol). The effects of the anti-anxiety drugs in the brain suggest hypotheses concerning the neural substrate of anxiety. Although the benzodiazepines and barbiturates facilitate the effects of gamma-aminobutyrate, this is insufficient to explain their highly specific behavioural effects. Because of similarities between the behavioural effects of certain lesions and those of the anti-anxiety drugs, it is proposed that these drugs reduce anxiety by impairing the functioning of a widespread neural system including the septo-hippocampal system, the Papez circuit, the prefrontal cortex, and ascending monoaminergic and cholinergic pathways which innervate these forebrain structures. Analysis of the functions of this system suggests that it acts as a comparator: it compares predicted to actual sensory events and activates the outputs of the BIS when there is a mismatch or when the predicted event is aversive. The resulting theory is applied to the symptoms and treatment of anxiety in man.
通过心理药理学实验，“行为抑制系统”（BIS）的概念得以发展。该系统通过抑制正在进行的行为并增强对环境的唤醒和注意力，对新异刺激或与惩罚或无奖励相关的刺激做出反应。正是BIS的活动构成了焦虑，而抗焦虑药物（苯二氮䓬类、巴比妥类和酒精）可减轻这种活动。抗焦虑药物在大脑中的作用提示了有关焦虑神经基质的假说。尽管苯二氮䓬类和巴比妥类药物可增强γ-氨基丁酸的作用，但这不足以解释它们高度特异性的行为效应。由于某些脑损伤的行为效应与抗焦虑药物的行为效应相似，因此有人提出这些药物通过损害包括隔区-海马系统、帕佩兹环路、前额叶皮质以及支配这些前脑结构的上行单胺能和胆碱能通路在内的广泛神经系统的功能来减轻焦虑。对该系统功能的分析表明，它起着比较器的作用：它将预测的感觉事件与实际的感觉事件进行比较，并在出现不匹配或预测事件具有厌恶性时激活BIS的输出。由此产生的理论被应用于人类焦虑的症状和治疗。
