An integrative view of mammalian seasonal neuroendocrinology

This is the peer reviewed version of the following article: Dardente, H., Wood, S.H., Ebling, F. & Sáenz de Miera, C. (2019). An integrative view of mammalian seasonal neuroendocrinology. Journal of neuroendocrinology. Journal of Neuroendocrinology, 31(5), e12729, which has been published in final form at https://doi.org/10.1111/jne.12729. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.Seasonal neuroendocrine cycles that govern annual changes in reproductive activity, energy metabolism and hair growth are almost ubiquitous in mammals that have evolved at temperate and polar latitudes. Changes in nocturnal melatonin secretion regulating gene expression in the pars tuberalis (PT) of the pituitary stalk are a critical common feature in seasonal mammals. The PT sends signal(s) to the pars distalis of the pituitary to regulate prolactin secretion and thus the annual moult cycle. The PT also signals in a retrograde manner via thyroid‐stimulating hormone to tanycytes, which line the ventral wall of the third ventricle in the hypothalamus. Tanycytes show seasonal plasticity in gene expression and play a pivotal role in regulating local thyroid hormone (TH) availability. Within the mediobasal hypothalamus, the cellular and molecular targets of TH remain elusive. However, two populations of hypothalamic neurones, which produce the RF‐amide neuropeptides kisspeptin and RFRP3 (RF‐amide related peptide 3), are plausible relays between TH and the gonadotrophin‐releasing hormone‐pituitary‐gonadal axis. By contrast, the ways by which TH also impinges on hypothalamic systems regulating energy intake and expenditure remain unknown. Here, we review the neuroendocrine underpinnings of seasonality and identify several areas that warrant further research

Differential response patterns of kisspeptin and RFamide-related peptide to photoperiod and sex steroid feedback in the Djungarian hamster ( Phodopus sungorus )

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Testosterone-driven seasonal regulation of vasopressin and galanin in the bed nucleus of the Stria Terminalis of the Djungarian Hamster (phodopus Sungorus)

The sexually dimorphic vasopressin system of the bed nucleus of the stria terminalis (BNST) is the most sensitive neurotransmitter system regulated by sex steroids in rats and mice. In addition to vasopressin, the BNST neurons also express a second neuropeptide, galanin, whose expression also appears to be regulated by testosterone in laboratory rodents. Seasonal fluctuations of sex steroids in photoperiodic rodents feed back on the brain to regulate the expression of sex steroid sensitive genes. The seasonal rhythm of circulating sex steroids is generated by photoperiod-controlled melatonin secretion, resulting in a seasonal stimulation and involution of the gonads. We have studied the seasonal expression of vasopressin and galanin in BNST neurons and their target areas in the Djungarian hamster (Phodopus sungorus). Furthermore, we analyzed the effect of testosterone on vasopressin and galanin by testosterone supplementation in animals where reproduction was inhibited by exposure to a short photoperiod. Exposure to short photoperiod induced a major reduction in the expression of vasopressin in BNST neurons, as well as in their target areas, the lateral septum (LS) and the lateral habenula (LHb). Galanin expression in the BNST and its target areas was also strongly reduced, although this reduction did not result in an almost complete disappearance of the neuropeptide as observed for vasopressin. Testosterone was able to reverse this reduction for both vasopressin and galanin. However, while the mRNA expression in BNST neurons recovered within 2-4 days, recovery of the neuropeptide immunoreactivity in the target areas, LS and LHb, required more than 3 weeks. The photoperiod-driven testosterone rhythm thus appears to be a major regulator of extra-hypothalamic vasopressin and galanin in the Djungarian hamster. The long delay between mRNA recovery in the cell body and the neuropeptide recovery in the target areas may be due to progressive filling up of the axon terminals. Alternatively, this delay might be indicative of a seasonal structural plasticity.14 page(s