However, it is unclear if melanopsin increases risk of SAD by causing differences in sleep or circadian phase, or if those differences are symptoms of the mood disorder.
Other studies reported on mRGCs in glaucoma, on genetic variation of the melanopsin gene (OPN4) in seasonal affective disorder and on the role of mRGCs in migraineous photophobia.
Temperament dimensions did not, however, differ significantly between carriers of different (dominant vs. recessive) alleles for the 5-HT(2A)T102C polymorphism in SAD patients.
Two genetic variants related to serotonergic transmission, the 5-HTTLPR and the 5-HT(2A)-1438G/A gene promoter polymorphisms, have been found to be associated with SAD.
5-HTT turnover rate, a measure for the number of inward transport events per minute, and tyramine-induced, 5-HTT-mediated outward transport were assessed at baseline, after 4 weeks of bright light therapy, and in summer using a case-control design in a consecutive sample of 73 drug-free depressed patients with SAD and 70 nonseasonal healthy controls.