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      Cells co-expressing luteinising hormone and thyroid-stimulating hormone are present in the ovine pituitary pars distalis but not the pars tuberalis: implications for the control of endogenous circannual rhythms of prolactin.

      1 , ,
      Neuroendocrinology
      S. Karger AG

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          Abstract

          A mammalian circannual pacemaker responsible for regulating the seasonal pattern of prolactin has been recently described in sheep. This pacemaker resides within the pars tuberalis, an area of the pituitary gland that densely expresses melatonin receptors. However, the chemical identity of the cell type which acts as the pacemaker remains elusive. Mathematical-modelling approaches have established that this cell must be responsive to the static melatonin signal as well as prolactin negative feedback. Considering that in sheep the gonadotroph is the only cell in the pars tuberalis which expresses the prolactin receptor, and that in other photoperiodic species the thyrotroph is the only cell expressing the melatonin receptor in this tissue, a cell type which expresses both proteins would fulfil the theoretical criteria of a circannual pacemaker.

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          Most cited references35

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          Thyrotrophin in the pars tuberalis triggers photoperiodic response.

          Molecular mechanisms regulating animal seasonal breeding in response to changing photoperiod are not well understood. Rapid induction of gene expression of thyroid-hormone-activating enzyme (type 2 deiodinase, DIO2) in the mediobasal hypothalamus (MBH) of the Japanese quail (Coturnix japonica) is the earliest event yet recorded in the photoperiodic signal transduction pathway. Here we show cascades of gene expression in the quail MBH associated with the initiation of photoinduced secretion of luteinizing hormone. We identified two waves of gene expression. The first was initiated about 14 h after dawn of the first long day and included increased thyrotrophin (TSH) beta-subunit expression in the pars tuberalis; the second occurred approximately 4 h later and included increased expression of DIO2. Intracerebroventricular (ICV) administration of TSH to short-day quail stimulated gonadal growth and expression of DIO2 which was shown to be mediated through a TSH receptor-cyclic AMP (cAMP) signalling pathway. Increased TSH in the pars tuberalis therefore seems to trigger long-day photoinduced seasonal breeding.
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            Ancestral TSH mechanism signals summer in a photoperiodic mammal.

            In mammals, day-length-sensitive (photoperiodic) seasonal breeding cycles depend on the pineal hormone melatonin, which modulates secretion of reproductive hormones by the anterior pituitary gland [1]. It is thought that melatonin acts in the hypothalamus to control reproduction through the release of neurosecretory signals into the pituitary portal blood supply, where they act on pituitary endocrine cells [2]. Contrastingly, we show here that during the reproductive response of Soay sheep exposed to summer day lengths, the reverse applies: Melatonin acts directly on anterior-pituitary cells, and these then relay the photoperiodic message back into the hypothalamus to control neuroendocrine output. The switch to long days causes melatonin-responsive cells in the pars tuberalis (PT) of the anterior pituitary to increase production of thyrotrophin (TSH). This acts locally on TSH-receptor-expressing cells in the adjacent mediobasal hypothalamus, leading to increased expression of type II thyroid hormone deiodinase (DIO2). DIO2 initiates the summer response by increasing hypothalamic tri-iodothyronine (T3) levels. These data and recent findings in quail [3] indicate that the TSH-expressing cells of the PT play an ancestral role in seasonal reproductive control in vertebrates. In mammals this provides the missing link between the pineal melatonin signal and thyroid-dependent seasonal biology.
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              Rapid sensing of circulating ghrelin by hypothalamic appetite-modifying neurons.

              To maintain homeostasis, hypothalamic neurons in the arcuate nucleus must dynamically sense and integrate a multitude of peripheral signals. Blood-borne molecules must therefore be able to circumvent the tightly sealed vasculature of the blood-brain barrier to rapidly access their target neurons. However, how information encoded by circulating appetite-modifying hormones is conveyed to central hypothalamic neurons remains largely unexplored. Using in vivo multiphoton microscopy together with fluorescently labeled ligands, we demonstrate that circulating ghrelin, a versatile regulator of energy expenditure and feeding behavior, rapidly binds neurons in the vicinity of fenestrated capillaries, and that the number of labeled cell bodies varies with feeding status. Thus, by virtue of its vascular connections, the hypothalamus is able to directly sense peripheral signals, modifying energy status accordingly.
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                Author and article information

                Journal
                Neuroendocrinology
                Neuroendocrinology
                S. Karger AG
                1423-0194
                0028-3835
                2013
                : 97
                : 4
                Affiliations
                [1 ] Department of Anatomy, Faculty of Medical and Veterinary Sciences, University of Bristol, Bristol, UK.
                Article
                000350790
                10.1159/000350790
                23548370
                7155b548-b1b6-4f0d-8cb3-caec69c66349
                History

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