Abstract
Photoperiod or the duration of daylight has been implicated as a risk factor in the development of mood disorders. The dopamine and serotonin systems are impacted by photoperiod and are consistently associated with affective disorders. Hence, we evaluated, at multiple stages of postnatal development, the expression of key dopaminergic (TH) and serotonergic (Tph2, SERT, and Pet-1) genes, and midbrain monoamine content in mice raised under control Equinox (LD 12:12), Short winter-like (LD 8:16), or Long summer-like (LD 16:8) photoperiods. Focusing in early adulthood, we evaluated the midbrain levels of these serotonergic genes, and also assayed these gene levels in the dorsal raphe nucleus (DRN) with RNAScope. Mice that developed under Short photoperiods demonstrated elevated midbrain TH expression levels, specifically during perinatal development compared to mice raised under Long photoperiods, and significantly decreased serotonin and dopamine content throughout the course of development. In adulthood, Long photoperiod mice demonstrated decreased midbrain Tph2 and SERT expression levels and reduced Tph2 levels in the DRN compared Short photoperiod mice. Thus, evaluating gene × environment interactions in the dopaminergic and serotonergic systems during multiple stages of development may lead to novel insights into the underlying mechanisms in the development of affective disorders.
Highlights
Photoperiod or the duration of daylight has been implicated as a risk factor in the development of mood disorders
By utilizing quantitative RTPCR we evaluated the expression levels of these dopamine and serotonin genes at postnatal days (P) 8, 18, and 35 in mice that continuously developed under control Equinox, Long summer-like, or Short winter-like photoperiod conditions from embryonic day 0 (E0) (Fig. 1)
In this study we evaluated the effects of photoperiod during key periods of postnatal development on gene expression levels and midbrain monoamine content in the dopaminergic and serotonergic systems
Summary
Photoperiod or the duration of daylight has been implicated as a risk factor in the development of mood disorders. Exposures to environmental factors during sensitive periods of development have been associated with elevated risk for neurodevelopmental disorders later in adulthood[8] To this point, studies have demonstrated significant development × environment effects resulting in increased prevalence for psychiatric d isorders[9]. Rodent studies in the dopaminergic and serotonergic systems have shown that photoperiodic exposure significantly affects neuronal firing rate[15,32], monoamine signaling[33,34,35], and mood-related behaviors[17,36,37], which can be sex-dependent[34,38]. Mice that developed under Long summer-like photoperiods demonstrate increased dorsal raphe (DRN) serotonin (5-HT) neuronal firing rate, elevated midbrain serotonin content, and reduced anxiety and depressive-like behaviors later in life in a melatonin receptor 1 (MT1R) dependent m anner[15]. Our lab has recently shown that prenatal photoperiodic exposure results in enduring changes to DRN 5-HT neuronal activity, and there are critical temporal windows within perinatal development that are impacted by photoperiod resulting in enduring changes to monoamine signaling and affective behaviors during adolescence and early adulthood[34]
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