NEUROBIOLOGY OF SEASONAL AFFECTIVE DISORDER AND LIGHT THERAPY

我们试图澄清季节性情感的病理生理学 障碍(SAD)和光疗(LT)的作用机制 下丘脑-垂体-肾上腺(HPA)对促肾上腺皮质激素的钝化反应 促肾上腺皮质激素释放激素(CRH)和5-羟色胺激动剂m-CPP和爱普沙酮；昼夜节律异常低 血浆催乳素水平&光疗降低夜间核心体型 温度。以下是过去一年进行的研究。A)试验性 光周期的改变影响垂体腺体积 非季节性抑郁症的增加。要评估PV是否在 悲伤患者(PTS)和对照组(CTS)，以及跨季节，受试者接受 磁共振成像。PTS AS的PGV无明显差异 与CTS相比，或跨季节。与SAD无关，PGV在 从冬季到夏季，女性减少，但男性减少。B)降低贝塔密度-- 白细胞膜制剂中的肾上腺素能受体存在于 抑郁症患者(非季节性)&与抑郁症的严重程度相关 暗示着信号转导的减少。以评估是否相同 发生在PTS中，我们评估了单核细胞G蛋白，它在 CTS和PTS的受体后信息转导及临床状态 目前的SAD，在LT治疗2-8周后再次出现。所有尺寸现在都是 在夏季重复，&数据分析将随之而来。C)临时秘书处经常 暴饮暴食，体重增加，渴望碳水化合物，血糖升高 摄入葡萄糖贷款后的胰岛素水平，非胰岛素的特征 我们测量了糖化血红蛋白(HbA1)水平。我们 预测PTS的HbA1水平将高于CTS，& 在冬季发现是这样的-但PTS水平在正常范围内 射程。我们在夏季重复测量，以评估季节是否 影响HbA1及HbA1与夏季症状缓解的关系。d) 核心体温在不同季节都有下降，但与 睡眠结构尚不清楚，因为睡眠有核心温度 调节功能。夜间脑电和核心电、面部和手部温度 冬季和夏季进行了测量。结果重复了我们的发现，即PTS 与CTS相比，其核心温度和手部温度相似。根本没有 PTS或CTS中温度的季节变化。PTS面部下部 不同季节的气温和面部温度都有所下降 PTS和CTS都有季节。面部温度在不同季节降低 PTS支持我们的假设，即光照和夏季与 大脑温度降低&可能会产生大脑热量。脑电数据 等待分析。E)早些时候，我们报告了夜间TSH、T3、T4的增加 无论临床状态如何，冬季PTS患者均出现T3倒置。在那 研究样本量有限&研究结果可能反映了 这些变量的节奏，而不是绝对的增加。因此，我们 已经从19个PTS和19个CTS整夜采集了新的样本。 分析工作正在进行中。

Our attempts to clarify the pathophysiological of seasonal affective disorder (SAD) & mechanisms of action of light therapy (LT), have shown blunted hypothalamo-pituitary-adrenal (HPA) responses to corticotrophin (CRH) & serotonin agonists m-CPP & ipsapirone; abnormally low circadian plasma prolactin levels & that light therapy reduces nocturnal core body temperature. Research conducted this past year follows. A) Experimental alteration of photoperiod affects pituitary gland volume (PGV), & PGV increases in non-seasonal depression. To assess whether PV changes among SAD patients (PTS) & controls (CTS), & across seasons, subjects underwent magnetic resonance imaging. There were no differences in PGV in PTS as compared to CTS, or across seasons. Independent of SAD, PGV increased in women but decreased in men winter to summer. B) Reduced density of beta- adrenergic receptors in leukocytes membrane preparations occurs in depressed patients (nonseasonal) & is correlated with depression severity suggesting a reduction in signal transduction. To assess whether the same occurs in PTS, we evaluated mononucleocyte G-proteins, which function in post receptor information transduction, & clinical state, in CTS & PTS with current SAD, &again at 2 & 8 weeks on LT. All measurements are now being repeated in summer, & data analysis will follow. C) PTS often overeat & gain weight, crave carbohydrates & have elevated glucose & insulin levels after glucose loan intake, features found with non-insulin resistance, we measured glycosylated hemoglobin (HbA1) levels. We predicted that PTS would have higher HbA1 levels as compared to CTS, & during winter found this to be so - but PTS levels were within a normal range. We are repeating measurements in summer to assess whether season affects HbA1 & relationship of HbA1 to summer symptom remission. D) Reduced core body temperature is observed across seasons but association with sleep architecture is unclear, as sleep has core temperature regulating functions. Nocturnal EEG & core, facial & hand temperatures were measured winter & summer. Results replicated our finding that PTS as compared to CTS had similar core & hand temperatures. There was no change in temperature across seasons in PTS or CTS. PTS had lower facial temperatures across seasons & facial temperatures decreased across seasons in both PTS & CTS. Reduced facial temperatures across seasons in PTS supports our hypothesis that light treatment & summer are related to decreased brain temperatures & possibly brain heat production. EEG data awaits analysis. E) Earlier we reported increased nocturnal TSH, T3, T4 and reverse T3 in PTS in winter, regardless of clinical status. In that study sample size was limited & the findings could reflect a shift in the rhythm of these variables rather than an absolute increase. Hence, we have drawn new samples throughout the night from 19 PTS & 19 CTS. Analysis is underway.