Abstract
Early life stimuli during critical developmental time frames have been linked to increased risk for neurodevelopmental disorders later in life. The serotonergic system of the brain is implicated in mood disorders and is impacted by the duration of daylight, or photoperiod. Here we sought to investigate sensitive periods of prenatal and postnatal development for photoperiodic programming of DRN serotonin neurons, midbrain serotonin and metabolite levels along with affective behaviors in adolescence (P30) or adulthood (P50). To address these questions we restricted the interval of exposure to prenatal development (E0-P0) for Long summer-like photoperiods (LD 16:8), or Short winter-like photoperiods (LD 8:16) with postnatal development and maturation then occurring under the opposing photoperiod. Prenatal exposure alone to Long photoperiods was sufficient to fully program increased excitability of DRN serotonin neurons into adolescence and adulthood, similar to maintained exposure to Long photoperiods throughout development. Interestingly, Long photoperiod exposure can elevate serotonin and its’ corresponding metabolite levels along with reducing affective behavior, which appear to have both pre and postnatal origins. Thus, exposure to Long photoperiods prenatally programs increased DRN serotonin neuronal excitability, but this step is insufficient to program serotonin signaling and affective behavior. Continuing influence of Long photoperiods during postnatal development then modulates serotonergic content and has protective effects for depressive-like behavior. Photoperiodic programing of serotonin function in mice appears to be a sequential process with programing of neuronal excitability as a first step occurring prenatally, while programing of circuit level serotonin signaling and behavior extends into the postnatal period.
Highlights
Exposure to environmental factors during key neurodevelopmental time points such as gestation and postnatal development have been associated with increased risk for psychiatric disorders later in life (Nestler et al, 2002; Andersen, 2015)
To test for the lasting effects of prenatal photoperiod exposure on dorsal raphe nucleus (DRN) serotonin neuron activity, mice were maintained on Long photoperiods from embryonic day 0 (E0) to birth (P0) and transferred to Short photoperiods until electrophysiological assays were performed at P30 or P50 (L-S cohort, Figure 1D), or exposed to Short photoperiods during gestation and transferred to Long photoperiods at birth and maintained there until assayed at P30 or P50 (S-L cohort, Figure 1E)
These spike rates were not statistically distinguishable, when using Holm-Sidak’s multiple comparison tests, from those exposed to Short photoperiods or to Long photoperiods throughout gestation, postnatal development, and maturation (L vs. summer-like photoperiods at birth (S-L), p = 0.2914, S vs. S-L, p = 0.1833, Figure 2B) suggesting that gestational exposure to Short photoperiods may prolong the sensitive period for programing excitability into early postnatal development
Summary
Exposure to environmental factors during key neurodevelopmental time points such as gestation and postnatal development have been associated with increased risk for psychiatric disorders later in life (Nestler et al, 2002; Andersen, 2015). Developmental photoperiod exposure was shown to drive the increased firing rate of dorsal raphe serotonin neurons in adulthood (Green et al, 2015). These findings suggest that there are sensitive periods during development during which photoperiod acts to program the serotonergic system relevant to the pathology of mood disorders
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