NEUROBIOLOGY OF SEASONAL AFFECTIVE DISORDER

季节性情感障碍的神经生物学

• 批准号: 4696480
• 负责人: N E ROSENTHAL
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF MENTAL HEALTH
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/4696480
• 关键词: REM sleep; basal metabolism; bioperiodicity; blood chemistry; circadian rhythms; cortisol; diagnostic tests; glucose tolerance test; human subject; hypoglycemia; melatonin; neuroendocrine system; phototherapy; psychophysiology; psychosomatic disorders; seasons; serotonin; sleep; sleep disorders; steroid hormone biosynthesis; steroid hormone metabolism; thyrotropin; urinalysis

As we have described elsewhere, patients with seasonal affective disorder (SAD) have annually occurring cycles of depression in fall and winter alternating with euthymia or hypomania occurring in the spring or summer. In the past we have investigated the neurobiology of patients with SAD by studying their sleep and neuroendocrine functioning. We have found that they sleep longer and have reduced delta sleep in the winter, as compared with the summer. However, dexamethasone suppression of cortisol secretion and TSH release in response to externally injected TRH appear normal. This past year our neurobiological investigations have revolved around melatonin metabolism in SAD. Blood was drawn over a 48-hour period in 7 SAD patients and 7 normal volunteers both in summer and in winter in order to establish the pattern of melatonin secretion in patients and normals. In addition, the melatonin precursor, 5-hydroxy-tryptamine was administered orally to 10 patients and 10 normal volunteers in the winter months and blood was drawn over a 5 hour period for melatonin analysis. We hypothesized that perhaps SAD is characterized by melatonin overproduction and that such a load of melatonin precursor would result in greater production of melatonin in patients than in normals. The melatonin specimens have yet to be analyzed.

正如我们在其他地方所描述的，季节性情感障碍患者 (SAD)每年秋季和冬季都会出现抑郁症的周期 在春季或夏季交替出现情绪正常或轻度躁狂。 在过去，我们通过以下方法研究了SAD患者的神经生物学： 研究他们的睡眠和神经内分泌功能。 我们发现 他们睡得更久，在冬天减少了三角睡眠， 随着夏天的到来。 然而，地塞米松抑制皮质醇分泌 和促甲状腺激素释放反应外部注射TRH似乎正常。 在过去的一年里，我们的神经生物学研究围绕着 SAD患者的褪黑素代谢。 在7例受试者中， SAD患者和7名正常志愿者在夏季和冬季分别进行了 以建立患者和正常人的褪黑激素分泌模式。 此外，给予褪黑激素前体5-羟色胺， 在冬季月份口服给10名患者和10名正常志愿者， 在5小时内抽血用于褪黑激素分析。 我们 假设SAD的特征可能是褪黑激素过度分泌 并且这样的褪黑激素前体负荷将导致更大的 患者的褪黑激素分泌量比正常人高。 褪黑激素 标本还有待分析。