Monoaminergic function in the pathogenesis of seasonal affective disorder

Abstract

Seasonal affective disorder\winter type (SAD) is characterized by recurrent depressive episodes during autumn and winter alternating with non-depressive episodes during spring and summer. Light therapy with fullspectrum, bright white light has been shown to be effective for this condition. Several hypotheses have been discussed in the literature about the pathogenesis of SAD. The most prominent includes disturbances in central monoaminergic transmission. Evidence can be inferred from studies showing a seasonal rhythm of central and peripheral serotonergic functioning which may be a predisposing factor for SAD. Some of the symptoms of SAD are believed to represent an attempt to overcome a putative deficit in brain serotonergic transmission. Moreover, 5-HT receptor challenge studies suggest altered activity at or downstream to central 5-HT receptors. Monoamine depletion studies support hypotheses about serotonergic and catecholaminergic dysfunctions in SAD and suggest that light therapy may well compensate for this underlying deficit. Further, albeit indirect, support for the importance of monoaminergic mechanisms in SAD and its involvement in the mechanism of the action of light therapy comes from studies showing antidepressant efficacy of serotonergic and noradrenergic antidepressants in the treatment of SAD. Altogether, disturbances in brain monoaminergic transmission seem to play a key role in the pathogenesis of SAD ; monoaminergic systems may also play an important role in the mechanisms of the action of light therapy.

G-Protein β₃ Subunit C825T Polymorphism Tends to Be Associated with Seasonal Variation in Young Male College Students

“…Using Kasper's criteria [13] , 16.4% of our sample were classifi ed as having SAD (winter: 11.6%, summer: 4.2%, fall: 0.53%, spring 0%) and 10.1% as having subsyndromal SAD (winter: 5.9%, summer: 2.7%, fall: 2.1%, spring: 0%). Thus, 26.5% is denoted henceforth 'seasonals'.…”

“…[10] suggested that light may exert its effects via normalization of transducin (a G-protein in the retina) levels, which are thought to be reduced in winter depression. The regulation of serotonergic neurotransmission is found to be altered in SAD, which also involves signal transduction via G-proteins [16] . Therefore, it is possible that the altered G-protein signal transduction related with the 825T allele and G ␤ 3s variant could mediate the response to light leading to seasonal variation and the pathophysiology of SAD.…”

Autumn Peak in Shooting Suicides of Children and Adolescents from Northern Finland

“…Seasonal affective disorder (SAD) is a condition of regularly occurring depressions, beginning in autumn or early winter, with a remission the following spring or summer [36] . Several hypotheses on the pathophysiology of SAD have been proposed, all of which stress the role of decreasing amounts of daylight during the autumn and winter season [36][37][38][39] . Further, there is a marked seasonality in brain serotonin levels with lowest serotonin content in the hypothalamus during the winter season, and changes in the function or effectiveness of serotonin have been suggested to be of importance in the pathogenesis of SAD [38] .…”

Transcranial Light Alters Melanopsin and Monoamine Production in Mouse (Mus musculus) Brain

“…The amount of OPN4 in the cerebellum was 1.21-fold higher in the EL group (P < 0.01), but no differences Transcranial Light Alters Circadian Molecules J Neurol Res. 2017;7(3): [39][40][41][42][43][44][45] were seen in the ML group compared to controls. Additionally, compared to the ML group, the amount of OPN4 was 1.55-fold higher in the EL group (P < 0.001) (Fig.…”

“…Additionally, monoamines play a role in light signaling [40], and also e.g. in SAD symptoms [41]. In order to determine whether transcranial light has direct effects on OPN4 and monoamine expression in the brain at different times of the day, we illuminated mice transcranially either in the morning or in the evening.…”