To understand mood disorders, we must hope to understand seasonality. Finally, we will propose particular inquiries where more research is needed to explore and validate these theories. Peculiar aspects of the induction of mania by bright light or sleep restriction suggest a theory that mania may be promoted by bifurcation of the circadian phasing of neuronal firing in two distinct populations of SCN neurons. Inadequate hypothalamic T3 may cause depression, whereas excessive hypothalamic T3 may mediate mania. We propose that this same mechanism may be a key controller of mood. These PT products then influence pituitary hormones and induce deiodinase 2 (DIO2), increasing hypothalamic triiodothyronine (T3), which maintains seasonal gonadal fertility. Melatonin offset influences thyrotropin (TSH) and tuberalin hormone synthesis by the PTĦ. In mammals, an exquisite mechanism in the pars tuberalis (PT) interprets daylength (photoperiod) from the duration of nocturnal melatonin secretion and particularly from the early morning termination time of secretion. The seasonal timing of daily light exposures reorganizes cellular circadian clocks in the bilateral suprachiasmatic nuclei (SCN) of the hypothalamus above the optic chiasm to regulate the evening rise and duration of melatonin secretionĤ.
In this presentation, we review the seasonality of mood disorders and the photoperiodic control of seasonality among mammals, in order to present new theories of the causes of depression and mania.
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