Manji H, Brown J H
Department of Psychiatry, University of British Columbia, Vancouver.
Can J Psychiatry. 1987 Dec;32(9):788-97. doi: 10.1177/070674378703200913.
This paper reviews briefly the very common finding in chronic antidepressant use, of subsensitivity of the beta-adrenoreceptor-linked cyclic AMP system. This subsensitivity is observed with a number of different antidepressant treatments, including pharmacological, electrical and sleep deprivation. The subsensitivity requires intact noradrenergic and serotonergic systems, functionally linking the two neurotransmitters most often implicated in depression. Thyroid hormones and estrogens also cause subsensitivity, while the opposite effect is seen with Reserpine and Propranolol. A modified conditioning/sensitization model is proposed, implicating psychosocial stressors with a biological inability to down-regulate beta-adrenoreceptors.
本文简要回顾了长期使用抗抑郁药时常见的一种现象，即β-肾上腺素能受体相关环磷酸腺苷系统的敏感性降低。在多种不同的抗抑郁治疗中都观察到了这种敏感性降低，包括药物治疗、电休克治疗和睡眠剥夺。这种敏感性降低需要完整的去甲肾上腺素能和血清素能系统，在功能上连接了抑郁症中最常涉及的两种神经递质。甲状腺激素和雌激素也会导致敏感性降低，而利血平和普萘洛尔则会产生相反的效果。本文提出了一种改良的条件反射/敏感化模型，认为社会心理应激源与生物性下调β-肾上腺素能受体的能力不足有关。
