Endocrine mechanisms of seasonal adaptation in small mammals: from early results to present understanding

Abstract

Seasonal adaptation is widespread among mammals of temperate and polar latitudes. The changes in physiology, morphology and behaviour are controlled by the photoneuroendocrine system that, as a first step, translates day lengths into a hormonal signal (melatonin). Decoding of the humoral melatonin signal, i.e. responses on the cellular level to slight alterations in signal duration, represents the prerequisite for appropriate timing of winter acclimatization in photoperiodic animals. Corresponding to the diversity of affected traits, several hormone systems are involved in the regulation downstream of the neural integration of photoperiodic time measurement. Results from recent studies provide new insights into seasonal control of reproduction and energy balance. Most intriguingly, the availability of thyroid hormone within hypothalamic key regions, which is a crucial determinant of seasonal transitions, appears to be regulated by hormone secretion from the pars tuberalis of the pituitary gland. This proposed neuroendocrine pathway contradicts the common view of the pituitary as a gland that acts downstream of the hypothalamus. In the present overview of (neuro)endocrine mechanisms underlying seasonal acclimatization, we are focusing on the dwarf hamster Phodopus sungorus (long-day breeder) that is known for large amplitudes in seasonal changes. However, important findings in other mammalian species such as Syrian hamsters and sheep (short-day breeder) are considered as well.

Thyroid hormone status affects expression of daily torpor and gene transcription in Djungarian hamsters (Phodopus sungorus)

“…A wellstudied seasonal animal model is the Djungarian hamster (also known as Siberian hamster, Phodopus sungorus, that reduces energetic costs during winter by shutting down reproduction, decreasing body mass, increasing fur insulation and the capacity for non-shivering thermogenesis in BAT (Heldmaier and Steinlechner, 1981a;Kauffman et al, 2001;Rafael et al, 1985;Scherbarth and Steinlechner, 2010). T3 availability to the hypothalamus has been shown to be a major driver of seasonal physiological adaptations (Ebling and Barrett, 2008;Hanon et al, 2008;Herwig et al, 2013Herwig et al, , 2009Nakao et al, 2008;Ross et al, 2011).…”

Melatonin Receptor 1 Deficiency Affects Feeding Dynamics and Pro-Opiomelanocortin<b> </b>Expression in the Arcuate Nucleus and Pituitary of Mice

“…Melatonin, the neurohormone of darkness produced in and secreted from the pineal organ, is a key messenger for the phase and the length of the night and trans-duces photoperiodic information [1] influencing the functional activity of the mediobasal hypothalamus and the adenohypophysis [2][3][4] . In general, melatonin can act upon two high-affinity melatonin receptors, MT1 and MT2 (formerly Mel1a and Mel1b) [5][6][7][8] .…”

Seasonal leptin resistance is associated with impaired signalling via JAK2-STAT3 but not ERK, possibly mediated by reduced hypothalamic GRB2 protein

“…Since the PT has a very high density of melatonin receptors, differential phospho-ERK ir within the PT may provide the molecular link between the pineal hormone melatonin, as the neuroendocrine transducer of the photoperiod signal, on the one hand and signalling mechanisms triggering seasonal changes in energy balance on the other hand. The PT has been well characterised as an important structure for seasonal changes in body weight (Scherbarth and Steinlechner 2010;Schuster et al 2000;Wagner et al 2007). Future studies are needed to resolve the molecular mechanism behind these interesting observations.…”