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.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Intramural Research (Z01)
Project #
1Z01MH002206-07
Application #
3859875
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
7
Fiscal Year
1991
Total Cost
Indirect Cost
Name
U.S. National Institute of Mental Health
Department
Type
DUNS #
City
State
Country
United States
Zip Code