Henley W N, Koehnle T J
Department of Biological Sciences, Ohio University, Athens 45701, USA.
Synapse. 1997 Sep;27(1):36-44. doi: 10.1002/(SICI)1098-2396(199709)27:1<36::AID-SYN4>3.0.CO;2-E.
Numerous clinical reports indicate that thyroid hormones can influence mood, and a change in thyroid status is an important correlate of depression. Moreover, thyroid hormones have been shown to be effective as adjuncts for traditional antidepressant medications in treatment-resistant patients. In spite of a large clinical literature, little is known about the mechanism by which thyroid hormones elevate mood. The lack of mechanistic insight reflects, in large part, a longstanding bias that the mature mammalian central nervous system is not an important target site for thyroid hormones. Biochemical, physiological, and behavioral evidence is reviewed that provides a clear picture of their importance for neuronal function. This paper offers the hypothesis that the thyroid hormones influence affective state via postreceptor mechanisms that facilitate signal transduction pathways in the adult mammalian brain. This influence is generalizable to widely recognized targets of antidepressant therapies such as noradrenergic and serotonergic neurotransmission.
众多临床报告表明，甲状腺激素可影响情绪，甲状腺状态的变化是抑郁症的一个重要相关因素。此外，在难治性患者中，甲状腺激素已被证明可作为传统抗抑郁药物的辅助药物发挥作用。尽管有大量临床文献，但对于甲状腺激素提升情绪的机制知之甚少。缺乏机制方面的见解在很大程度上反映了一种长期存在的偏见，即成熟的哺乳动物中枢神经系统不是甲状腺激素的重要靶位点。本文综述了生化、生理和行为方面的证据，这些证据清楚地表明了它们对神经元功能的重要性。本文提出假说，即甲状腺激素通过促进成年哺乳动物大脑中信号转导途径的受体后机制来影响情感状态。这种影响可推广到抗抑郁治疗广泛认可的靶点，如去甲肾上腺素能和5-羟色胺能神经传递。
