Abstract
Seasonal changes in light exposure have profound effects on behavioral and physiological functions in many species, including effects on mood and cognitive function in humans. The mammalian brain's master circadian clock, the suprachiasmatic nucleus (SCN), transmits information about external light conditions to other brain regions, including some implicated in mood and cognition. Although the detailed mechanisms are not yet known, the SCN undergoes highly plastic changes at the cellular and network levels under different light conditions. We therefore propose that the SCN may be an essential mediator of the effects of seasonal changes of day length on mental health. In this review, we explore various forms of neuroplasticity that occur in the SCN and other brain regions to facilitate seasonal adaptation, particularly altered phase distribution of cellular circadian oscillators in the SCN and changes in hypothalamic neurotransmitter expression.
Highlights
To adapt to changes in the light-dark environment, organisms have evolved an internal circadian clock that drives many behavioral and physiological outputs, such as daily cycles of sleep-wake, metabolism, hormone secretion, and cognitive function
The high rate of neurotransmitter coexpression displayed by suprachiasmatic nucleus (SCN) neurons even at baseline [33] suggests that they may already have in place whatever molecular machinery is required to express multiple neurotransmitter phenotypes [28]
It is clear that plasticity in circadian phase distribution among SCN neurons is the primary mechanism encoding seasonal adaptation, notably via photoperiod-dependent changes in duration of nocturnal secretion of the pineal hormone melatonin [32]. These findings suggest that environmental light conditions may influence mood and behavior through the SCN as well as other brain regions that receive intrinsically photosensitive retinal ganglion cells (ipRGCs) afferents
Summary
To adapt to changes in the light-dark environment, organisms have evolved an internal circadian (ca. 24 hr) clock that drives many behavioral and physiological outputs, such as daily cycles of sleep-wake, metabolism, hormone secretion, and cognitive function. An additional regulatory loop includes both positive and negative regulatory elements: retinoic acid-related orphan receptor ROR (α, β, and γ) and nuclear heme receptor REV-ERB (α and β), respectively [7, 8]. These molecular rhythms result in appropriately timed cycles of physiology, metabolism, and behavior. SCN neurons coordinate with one another to adapt the nucleus to different light environments, leading to highly plastic changes at the cellular and network levels. These changes may influence the activity of SCN targets. We will highlight studies that broaden our understanding of neuronal phenotype plasticity and related effects on circadian rhythms and behavior
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