NEUROBIOLOGY OF SEASONAL AFFECTIVE DISORDER AND LIGHT THERAPY

光对冬季SAD的作用机制及生物学特性 导致这种综合征的异常情况尚不清楚。我们一直在追查 SAD的眼、神经内分泌三条线的病理生理 档案和免疫生物学。以确认SAD患者是否 对光的感知超敏感，正如我们可能已经展示的那样，我们评估了 Goldmann/Weekers适配仪暗适应25例 以及25名年龄和性别匹配的对照组。我们发现两者之间没有区别 两组。DePue和其他人已经确定多巴胺是一种 季节性情感障碍(SAD)研究的神经递质。 在动物身上的研究已经证实，多巴胺是主要的 脊椎动物视网膜中的神经递质和视网膜的产生 多巴胺受光刺激，受视网膜产生的抑制 褪黑激素。特别是为了评估视网膜的多巴胺能机制，我们 对SAD患者和非SAD患者进行视网膜电信号和眨眼频率检查 用L多巴加卡比多巴治疗前后均为正常对照组。 图形视网膜电信号显示两者之间没有显著差异 患者和对照组在治疗前或治疗后。眼睛的分析 患者和对照组之间的眨眼率也没有差异。 然而，晨光治疗显著降低了眨眼率。 绝经前的女性。这一发现特别令人感兴趣 发现SAD患者多巴胺能失调的证据的研究人员 专门研究绝经前妇女。我们计划继续我们的 眼部可能的多巴胺能异常的研究 对冬季SAD患者和正常志愿者进行眼电描记。 我们对冬季SAD神经内分泌功能的研究表明 那道光纠正了这一反常现象。我们延续了我们之前的工作 SAD患者与配对人群免疫功能的比较 控制，但我们无法确定两组之间的任何差异 或任何光疗改变免疫参数的证据。

The mechanism of action of light for winter SAD and the biological abnormalities responsible for the syndrome are unknown. We have pursued the pathophysiology of SAD along three lines: the eye, neuroendocrine profiles, and immunobiology. To confirm whether patients with SAD are supersensitive to perceiving light, as we have probably shown, we evaluated dark adaptation by means of a Goldmann/Weekers Adaptometer on 25 patients and 25 age- and sex-matched controls. We found no difference between the two groups. Depue and others have identified dopamine as a neurotransmitter of research interest in seasonal affective disorder (SAD). Research in animals has established that dopamine is the major neurotransmitter in the vertebrate retina and that production of retinal dopamine is stimulated by light and suppressed by retinally-produced melatonin. To assess retinal dopaminergic mechanisms in particular, we examined electroretinograms and eye blink rates in SAD patients and in normal controls both before and after treatment with L-dopa plus carbidopa. Pattern electroretinograms showed no significant difference between patients and controls either before or after treatment. Analysis of eye blink rates also showed no differences between patients and controls. Nevertheless, morning light treatment significantly reduced eye blink rate in premenopausal females. This finding is of particular interest given that the researcher who found evidence of dopaminergic dysregulation in SAD exclusively studied premenopausal women. We plan to continue our investigation of possible eye-related dopaminergic abnormalities by performing electrooculograms on winter SAD patients and normal volunteers. Our investigations of neuroendocrine functioning in winter SAD have shown that light corrects this abnormality. We continued previous work of our group comparing immunological function among SAD patients and matched controls, but we were unable to establish any difference between the groups or any evidence of light therapy changing immune parameters.