Boulenger J P, Uhde T W
Encephale. 1982;8(2):119-30.
Anxiety is often accompanied by physiological and neuroendocrine changes in both psychiatric patients and normal volunteers. Among these correlates the increase of plasma cortisol and catecholamine concentrations have also been documented in stress and hyperarousal states and, therefore, their specificity in anxiety remains to be studied. Recent studies have shown that biological correlates of central noradrenergic system activity, measured in the CSF or blood are increased in relation to anxiety symptoms. Redmond (1979) has proposed a model for the study of anxiety based upon the function of the noradrenergic locus coeruleus (LC) which may provide a neuroanatomical basis for these changes. In the animal, electrical and pharmacological activation of the LC causes increased NE turnover and fear-associated behaviors, whereas lesions and pharmacologic inhibition of the LC produce decreased fear-associated behavior and NE turnover. Drugs with known antianxiety efficacy in man decrease the LC firing in animals. In contrast, clonidine, an alpha-2 adrenergic agonist which inhibits LC activity in animals may have antianxiety effects in patients with depression, anxiety, and opiate abstinence syndrome.
焦虑常常伴随着精神病患者和正常志愿者的生理及神经内分泌变化。在这些相关因素中，血浆皮质醇和儿茶酚胺浓度的升高在应激和高唤醒状态下也有记录，因此，它们在焦虑中的特异性仍有待研究。最近的研究表明，在脑脊液或血液中测量的中枢去甲肾上腺素能系统活动的生物学相关因素与焦虑症状有关。雷德蒙德（1979年）提出了一个基于去甲肾上腺素能蓝斑（LC）功能的焦虑研究模型，该模型可能为这些变化提供神经解剖学基础。在动物中，LC的电刺激和药物激活会导致去甲肾上腺素（NE）周转率增加以及与恐惧相关的行为，而LC的损伤和药物抑制会导致与恐惧相关的行为和NE周转率降低。在人类中具有已知抗焦虑功效的药物会降低动物的LC放电。相反，可乐定是一种α-2肾上腺素能激动剂，可抑制动物的LC活性，它可能对患有抑郁症、焦虑症和阿片类药物戒断综合征的患者有抗焦虑作用。
