neuropeptide-y and Seasonal-Affective-Disorder

The seasonality of depressive symptoms is prevalent in children and adolescents. However, the mechanisms that underlie such susceptibility to seasonal influences on mood disorders are unclear. We examined the effects of a short photoperiod condition on the susceptibility to subchronic unpredictable mild stress (SCUS) and rhythmic alterations of plasma corticosterone (CORT), melatonin, and neuropeptide Y (NPY) in adolescent male rats. Compared with the 12h/12h light/dark photoperiod control (CON) rats, the 8h/16h photoperiod SCUS rats exhibited significant anhedonia, a core symptom of human depression, together with a blunted diurnal rhythm and elevation of 24h CORT, melatonin, and NPY levels. The 8h/16h photoperiod condition also blunted the rhythmicity of CORT, caused a phase inversion of melatonin, and caused a phase delay of NPY compared with 12h/12h CON rats. Such abnormalities of plasma CORT, NPY, and melatonin might cause adolescent individuals to present higher stress reactivity and greater vulnerability to stress over their lifetimes. The present study provides evidence of the susceptibility to the seasonality of stress-related disorders in adolescence.

Topics: Aging; Anhedonia; Animals; Circadian Rhythm; Corticosterone; Disease Models, Animal; Disease Susceptibility; Male; Melatonin; Neuropeptide Y; Photoperiod; Rats, Sprague-Dawley; Resilience, Psychological; Seasonal Affective Disorder; Seasons; Stress, Psychological; Uncertainty

Noradrenaline, estrogen, neuropeptide Y and galanin are all involved in regulation of eating behaviour. Based on a recent case report on seasonal affective disorder (SAD), there is evidence of decreased insulin sensitivity. Reduced insulin sensitivity may increase the transcriptional activity of the neuropeptide Y gene in the medial basal hypothalamus and subsequent ingestion of food. Decreased availability of estrogen may also increase the levels of neuropeptide Y, leading to decreased release of noradrenaline from the ventromedial hypothalamus. The increased noradrenaline content may increase the concentration of galanin, which will decrease the circulating levels of insulin and increase the pace of transcription of the neuropeptide Y gene. Among some SAD patients, it is possible that the sustained ingestion of high-fat diet will rather activate the transcription of the neuropeptide Y gene than deactivate it, indicating a defect in macronutrient selection.

Topics: Animals; Eating; Estrogens; Galanin; Humans; Hypothalamus; Insulin Resistance; Models, Biological; Neuropeptide Y; Norepinephrine; Rats; Seasonal Affective Disorder