Abstract:The pars tuberalis (PT) of the adenohypophysis expresses a high density of melatonin receptors and is thought to be a crucial relay for the actions of melatonin on seasonal rhythmicity of prolactin secretion by the pars distalis (PD). In common with the suprachiasmatic nucleus of the hypothalamus and most other peripheral tissues, the PT rhythmically expresses a range of 'clock genes'. Interestingly, this expression is highly dependent upon melatonin/photoperiod, with several aspects unique to the PT. These ob… Show more
“…An example supporting this assumption is the pars tuberalis of the adenohypophysis whose expression of clock genes and proteins is timed by circulating melatonin (Jilg et al 2005;Dardente 2007). The rhythmic expression of PER2 has been reported in several limbic forebrain structures.…”
Section: Effects Of Meal Time On Extra-scn Cerebral Clock/oscillatorsmentioning
Daily brain rhythmicity, which controls the sleep-wake cycle and neuroendocrine functions, is generated by an endogenous circadian timing system. Within the multi-oscillatory circadian network, a master clock is located in the suprachiasmatic nuclei of the hypothalamus, whose main synchroniser (Zeitgeber) is light. In contrast, imposed meal times and temporally restricted feeding are potent synchronisers for secondary clocks in peripheral organs such as the liver and in brain regions, although not for the suprachiasmatic nuclei. Even when animals are exposed to a light-dark cycle, timed calorie restriction (i.e. when only a hypocaloric diet is given every day) is a synchroniser powerful enough to modify the suprachiasmatic clockwork and increase the synchronising effects of light. A daily chocolate snack in animals fed ad libitum with chow diet entrains the suprachiasmatic clockwork only under the conditions of constant darkness and decreases the synchronising effects of light. Secondary clocks in the brain outside the suprachiasmatic nuclei are differentially influenced by meal timing. Circadian oscillations can either be highly sensitive to food-related metabolic or reward cues (i.e. their phase is shifted according to the timed meal schedule) in some structures or hardly affected by meal timing (palatable or not) in others. Furthermore, animals will manifest food-anticipatory activity prior to their expected meal time. Anticipation of a palatable or regular meal may rely on a network of brain clocks, involving metabolic and reward systems and the cerebellum.
“…An example supporting this assumption is the pars tuberalis of the adenohypophysis whose expression of clock genes and proteins is timed by circulating melatonin (Jilg et al 2005;Dardente 2007). The rhythmic expression of PER2 has been reported in several limbic forebrain structures.…”
Section: Effects Of Meal Time On Extra-scn Cerebral Clock/oscillatorsmentioning
Daily brain rhythmicity, which controls the sleep-wake cycle and neuroendocrine functions, is generated by an endogenous circadian timing system. Within the multi-oscillatory circadian network, a master clock is located in the suprachiasmatic nuclei of the hypothalamus, whose main synchroniser (Zeitgeber) is light. In contrast, imposed meal times and temporally restricted feeding are potent synchronisers for secondary clocks in peripheral organs such as the liver and in brain regions, although not for the suprachiasmatic nuclei. Even when animals are exposed to a light-dark cycle, timed calorie restriction (i.e. when only a hypocaloric diet is given every day) is a synchroniser powerful enough to modify the suprachiasmatic clockwork and increase the synchronising effects of light. A daily chocolate snack in animals fed ad libitum with chow diet entrains the suprachiasmatic clockwork only under the conditions of constant darkness and decreases the synchronising effects of light. Secondary clocks in the brain outside the suprachiasmatic nuclei are differentially influenced by meal timing. Circadian oscillations can either be highly sensitive to food-related metabolic or reward cues (i.e. their phase is shifted according to the timed meal schedule) in some structures or hardly affected by meal timing (palatable or not) in others. Furthermore, animals will manifest food-anticipatory activity prior to their expected meal time. Anticipation of a palatable or regular meal may rely on a network of brain clocks, involving metabolic and reward systems and the cerebellum.
“…Diurnal rhythms of αGSU mRNA expression have also been demonstrated in the hamster par tuberalis (Arai and Kameda 2004). Thus, the pars tuberalis transduces photoperiodic changes and drives seasonal changes in prolactin secretion from the pars distalis (for reviews, see Dardente 2007).…”
The hypophyseal pars tuberalis surrounds the median eminence and infundibular stalk of the hypothalamus as thin layers of cells. The pars tuberalis expresses MT1 melatonin receptor and participates in mediating the photoperiodic secretion of pituitary hormones. Both the rostral tip of Rathke's pouch (pars tuberalis primordium) and the pars tuberalis expressed alphaGSU mRNA, and were immunoreactive for LH, chromogranin A, and TSHbeta in mice. Hes genes control progenitor cell differentiation in many embryonic tissues and play a crucial role for neurulation in the central nervous system. We investigated the Hes1 function in outgrowth and differentiation of the pars tuberalis by using the markers for the pars tuberalis. In homozygous Hes1 null mutant embryos, the rostral tip was formed in the basal-ventral part of Rathke's pouch at embryonic day (E)11.5 as well as in wild-type embryos. In contrast to the wild-type, the rostral tip of null mutants could not extend rostrally with age; it remained in the low extremity of Rathke's pouch during E12.5-E13.5 and disappeared at E14.5, resulting in lack of the pars tuberalis. Development of the ventral diencephalon was impaired in the null mutants at early stages. Rathke's pouch, therefore, could not link with the nervous tissue and failed to receive inductive signals from the diencephalon. In a very few mutant mice in which the ventral diencephalon was partially sustained, some pars tuberalis cells were distributed around the hypoplastic infundibulum. Thus, Hes1 is required for development of the pars tuberalis and its growth is dependent on the ventral diencephalon.
“…The description of sites of action of melatonin in the brain in the 1990s lead to the identification of a little studied proximal region of the pituitary gland, the pars tuberalis (PT) (reviewed in [7]). We now know that the PT is a major site of action of melatonin for the regulation of mammalian seasonal physiology [7,8]. This review focuses on the role of the photoperiodic processes driven by melatonin with a particular emphasis on the seasonal regulation of prolactin (PRL) secretion (fig.…”
In mammals, the nocturnal melatonin signal is well established as a key hormonal indicator of seasonal changes in day-length, providing the brain with an internal representation of the external photoperiod. The pars tuberalis (PT) of the pituitary gland is the major site of expression of the G-coupled receptor MT1 in the brain and is considered as the main site of integration of the photoperiodic melatonin signal. Recent studies have revealed how the photoperiodic melatonin signal is encoded and conveyed by the PT to the brain and the pituitary, but much remains to be resolved. The development of new animal models and techniques such as cDNA arrays or high throughput sequencing has recently shed the light onto the regulatory networks that might be involved. This review considers the current understanding of the mechanisms driving photoperiodism in the mammalian PT with a particular focus on the seasonal prolactin secretion.
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