Zacharko R M, Koszycki D, Mendella P D, Bradwejn J
Psychology Department, Carleton University, Ottawa, Ontario, Canada.
Prog Neurobiol. 1995 Nov-Dec;47(4-5):371-423.
Neurochemical accounts of panic disorder focus on peripheral indices of central transmitter activity, hormonal correlates and therapeutic efficacy. Anxiogenic agents augment norepinephrine activity, some anxiolytics increase serotonin neurotransmission while benzodiazepines and antidepressants influence catecholamine, indoleamine and gamma-aminobutyric acid turnover in infrahuman subjects. Reliable correlates of central transmitter activity in panic disorder are not in evidence. While animal models of anxiety may not mirror the symptom profile of panic, neurobiological accounts of panic disorder fail to consider extensive central colocalization of neurotransmitter and putative neurotransmitters. In effect, transmitter release in major ascending and descending transmitter systems is modulated by variable neuropeptide interfacing. The behavioral concomitants of psychological disturbance likely follow from variable neurochemical release induced by stimuli as well as conditioning and sensitization. The functional role of receptor sites associated with multiple neurochemical systems may vary and the sensitivity and/or density of receptor sites may be modified. Accordingly, the behavioral and neurochemical concomitants of acute and chronic pathology may be fundamentally different from one another. The present review argues that the symptoms of panic disorder and the etiology of the illness must be evaluated against a background of genetic, organismic and experiential factors. Such variables presumably underlie the diverse behavioral symptoms associated with panic disorder and variations in the therapeutic efficacy of pharmacological treatment.
惊恐障碍的神经化学解释聚焦于中枢递质活动的外周指标、激素相关性及治疗效果。致焦虑剂会增强去甲肾上腺素的活性，一些抗焦虑药会增加5-羟色胺神经传递，而苯二氮䓬类药物和抗抑郁药会影响非人类受试者体内儿茶酚胺、吲哚胺和γ-氨基丁酸的代谢。目前尚无惊恐障碍中枢递质活动的可靠相关证据。虽然焦虑的动物模型可能无法反映惊恐的症状特征，但惊恐障碍的神经生物学解释未能考虑神经递质和假定神经递质在中枢的广泛共定位。实际上，主要的上行和下行递质系统中的递质释放是由可变的神经肽相互作用调节的。心理障碍的行为伴随症状可能源于刺激以及条件作用和敏感化所诱导的可变神经化学释放。与多种神经化学系统相关的受体位点的功能作用可能不同，并且受体位点的敏感性和/或密度可能会发生改变。因此，急性和慢性病理状态的行为和神经化学伴随症状可能在根本上彼此不同。本综述认为，惊恐障碍的症状和病因必须在遗传、机体和经验因素的背景下进行评估。这些变量大概是与惊恐障碍相关的各种行为症状以及药物治疗疗效差异的基础。
