NEUROBIOLOGY OF SEASONAL AFFECTIVE DISORDER AND LIGHT THERAPY

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Although repeated studies have established that bright light is an effective treatment for SAD, the mechanisms of its actions remains unknown, as do the fundamental biological abnormalities responsible for the syndrome. There is ample reason to believe that brain serotonergic systems may be involved in these processes. Last year we reported that SAD patients respond abnormally, with exaggerated activation and euphoria, to infusions of the serotonin agonist, m-CPP. We have followed up this previous report on the hormonal and temperature responses of the same patients to this challenge study. This year we extended our research to test the hypothesis that serotonergic transmission is an important regulator of mood in SAD patients by attempting to reverse the antidepressant effects of light therapy and exacerbate depression i these same individuals by reducing brain serotonin levels. We attempted to accomplish this by manipulating dietary macronutrients to induce biochemical changes. We also studied peripheral markers of serotonin function by measuring parameters of platelet binding. Platelets respond to serotonin and antidepressant medications in plasma in a similar fashion as brain cells. A third study followed up on our previous study of the role of the eye and its connections to the brain in the pathogenesis of SAD, by comparing patients and controls in winter and summer conditions. Finally, a group of SAD patients an controls were studied in winter and summer in order to understand sympathetic nervous system response and the hypothalamo-pituitary-adrenal (HPA) axis. SAD patients and controls were given m-CPP or placebo infusions on separate days in untreated and light therapy treated conditions in a randomized block design. For 90 minutes following infusion blood was drawn for prolactin, cortisol, and ACTH. Core and peripheral body temperature were also taken. Plasma prolactin and cortisol levels showed a trend toward the previous findings (hypersecretion in SAD patients), but did not replicate those findings. no difference between patient and control group was found for core body temperature. Light treatment lowered overnight temperature in both groups. Patients had higher peripheral body temperature which rose towards normal levels during light therapy. In the platelet study no differences were found between SAD patients and controls in any of the measures and between light therapy conditions in SAD patient A group of SAD patients and controls in winter and summer were administered a standard ocular paradigm and an EOG was taken. A significant season y group difference was found (F=4.84, G-G p<.05) in which controls had a significantly higher EOG ratio in winter than patients or than in both groups in summer. The study of the sympathetic nervous system and HPA axis is ongoing, and as yet there are no findings.