Sulser F
Pharmakopsychiatr Neuropsychopharmakol. 1978 Jan;11(1):43-52. doi: 10.1055/s-0028-1094561.
The results provide evidence for a central postsynaptic regulatory mechanism involving the noradrenergic receptor coupled adenylate cyclase system. This particular system in the limbic forebrain displays properties of an adrenergic receptor with partial beta characteristics. Drugs which either can precipitate or alleviate depression in man cause time dependent opposite changes in the reactivity of this receptor system. It is tempting to speculate that depression-prone patients may have catecholamine receptors in limbic and possibly other brain structures with heightened responsiveness and that successful treatment requires desensitization of enhanced noradrenergic receptor function thus causing a reduction in the postulated amplificational mechanism that translates sensory input eventually into physiological and behavioral events.
这些结果为一种涉及去甲肾上腺素能受体偶联腺苷酸环化酶系统的中枢突触后调节机制提供了证据。边缘前脑的这一特定系统表现出具有部分β特性的肾上腺素能受体的特性。那些能够诱发或缓解人类抑郁症的药物会使该受体系统的反应性随时间发生相反的变化。很容易推测,易患抑郁症的患者在边缘系统以及可能的其他脑结构中可能具有反应性增强的儿茶酚胺受体,而成功的治疗需要使增强的去甲肾上腺素能受体功能脱敏,从而减少假定的将感觉输入最终转化为生理和行为事件的放大机制。