Gene expression profiling during hibernation in the European hamster.

Hibernation is an exceptional physiological response to a hostile environment, characterized by a seasonal period of torpor cycles involving dramatic reductions of body temperature and metabolism, and arousal back to normothermia. As the mechanisms regulating hibernation are still poorly understood, here we analysed the expression of genes involved in energy homeostasis, torpor regulation, and daily or seasonal timing using digital droplet PCR in various central and peripheral tissues sampled at different stages of torpor/arousal cycles in the European hamster. During torpor, the hypothalamus exhibited strongly down-regulated gene expression, suggesting that hypothalamic functions were reduced during this period of low metabolic activity. During both torpor and arousal, many structures (notably the brown adipose tissue) exhibited altered expression of deiodinases, potentially leading to reduced tissular triiodothyronine availability. During the arousal phase, all analysed tissues showed increased expression of the core clock genes Per1 and Per2. Overall, our data indicated that the hypothalamus and brown adipose tissue were the tissues most affected during the torpor/arousal cycle, and that clock genes may play critical roles in resetting the body's clocks at the beginning of the active period.

Maternal photoperiod programs hypothalamic thyroid status via the fetal pituitary gland.

In wild mammals, offspring development must anticipate forthcoming metabolic demands and opportunities. Within species, different developmental strategies may be used, dependent on when in the year conception takes place. This phenotypic flexibility is initiated before birth and is linked to the pattern of day length (photoperiod) exposure experienced by the mother during pregnancy. This programming depends on transplacental communication via the pineal hormone melatonin. Here, we show that, in the Siberian hamster (Phodopus sungorus), the programming effect of melatonin is mediated by the pars tuberalis (PT) of the fetal pituitary gland, before the fetal circadian system and autonomous melatonin production is established. Maternal melatonin acts on the fetal PT to control expression of thyroid hormone deiodinases in ependymal cells (tanycytes) of the fetal hypothalamus, and hence neuroendocrine output. This mechanism sets the trajectory of reproductive and metabolic development in pups and has a persistent effect on their subsequent sensitivity to the photoperiod. This programming effect depends on tanycyte sensitivity to thyroid stimulating hormone (TSH), which is dramatically and persistently increased by short photoperiod exposure in utero. Our results define the role of the fetal PT in developmental programming of brain function by maternal melatonin and establish TSH signal transduction as a key substrate for the encoding of internal calendar time from birth to puberty.

Opposite actions of hypothalamic vasopressin on circadian corticosterone rhythm in nocturnal versus diurnal species.

Relatively little is known about the function of the biological clock and its efferent pathways in diurnal species, despite the fact that its major transmitters and neuronal connections are also conserved in humans. The mammalian biological clock is located in the hypothalamic suprachiasmatic nuclei (SCN). Several lines of evidence suggest that the activity cycle of the SCN itself is similar in nocturnal and diurnal mammals. Previously, we showed that, in the rat, vasopressin (VP) derived from the SCN has a strong inhibitory effect on the release of adrenal corticosterone and is an important component in the generation of a daily rhythm in plasma corticosterone concentrations. In the present study we investigated the role of VP in the control of the daily corticosterone rhythm in a diurnal rodent, i.e. Arvicanthis ansorgei. Contrary to our previous (rat) results, VP administered to the hypothalamic paraventricular nucleus in A. ansorgei had a stimulatory effect on the release of corticosterone. Moreover, both the morning and evening rise in corticosterone were blocked by the administration of a VP receptor antagonist. These results show that with regard to the circadian control of the corticosterone rhythm in diurnal and nocturnal rodents, temporal information is carried along the same pathway from the SCN to its target areas, but the response of the target area may be quite different. We propose that the reversed response to VP is due to a change in the phenotype of the target neurons that are contacted by the SCN efferents, i.e. glutamatergic instead of gamma-aminobutyric acid (GABA)ergic.