Seasonal Morphological Changes in the Neuro-Glial Interaction between Gonadotropin-Releasing Hormone Nerve Terminals and Glial Endfeet in Japanese Quail

Yamamura, Takashi; Hirunagi, Kanjun; Ebihara, Shizufumi; Yoshimura, Takashi

doi:10.1210/en.2004-0366

Cited by 185 publications

(125 citation statements)

References 21 publications

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“…These include actions as leptin and glucose sensors relaying metabolic feedback signals to the arcuate nucleus (38,39) and as physical barriers controlling access of blood/CSF signals to the brain and release of hypothalamic neuropeptides to the pituitary portal system (40,41). Hence photoperiodic historydependent adjustment of tanycyte sensitivity to TSH constitutes an effective proximate mechanism to meet the ultimate evolutionary drive to exploit day length as a calendar synchronizer for annual life-history programs (Fig.…”

Section: Discussionmentioning

confidence: 99%

Maternal photoperiod programs hypothalamic thyroid status via the fetal pituitary gland

Miera

Bothorel

Jaeger

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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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.photoperiodism | developmental programming | hypothalamus | pars tuberalis | thyroid

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Section: Discussionmentioning

confidence: 99%

Maternal photoperiod programs hypothalamic thyroid status via the fetal pituitary gland

Miera

Bothorel

Jaeger

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…The internal layer of the ME corresponds to where some GnIH fiber terminals are located; it also corresponds to where many glia are (Yamamura et al, 2004). Thus, it is possible that GnIH (a) does not affect cGnRH-I release, (b) influences cGnRH-I release to the ME indirectly via action upon glial cells (Yamamura et al, 2004), or (c) acts directly on cGnRH-I fibers-just not at the terminal. Finally, the fact that an effect of GnIH was seen at 5 min does not preclude a more rapid effect via some other mechanism.…”

Section: Discussionmentioning

confidence: 99%

Rapid inhibition of female sexual behavior by gonadotropin-inhibitory hormone (GnIH)

Bentley

Jensen

Kaur

et al. 2006

Hormones and Behavior

167

119

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TitleRapid inhibition of female sexual behavior by gonadotropin-inhibitory hormone (GnIH). Abstract Gonadotropin-releasing hormone (GnRH) is largely responsible for the initiation of sexual behaviors; one form of GnRH activates a physiological cascade causing gonadal growth and gonadal steroid feedback to the brain, and another form is thought to act as a neurotransmitter to enhance sexual receptivity. In contrast to GnRH, gonadotropin-inhibitory hormone (GnIH) inhibits gonadotropin release. The distribution of GnIH in the avian brain suggests that it has not only hypophysiotropic actions but also unknown behavioral actions. GnIH fibers are present in the median eminence (ME) and are in apparent contact with chicken GnRH (cGnRH)-I and -II neurons and fibers. In birds, cGnRH-I regulates pituitary gonadotropin release, whereas cGnRH-II enhances copulation solicitation in estradiol-primed females exposed to male song. In the present study, we determined the effects of GnIH administered centrally to female white-crowned sparrows. A physiological dose of GnIH reduced circulating LH and inhibited copulation solicitation, without affecting locomotor activity. Using rhodaminated GnIH, putative GnIH binding sites were seen in the ME close to GnRH-I fiber terminals and in the midbrain on or close to GnRH-II neurons. These data demonstrate direct effects of GnIH upon reproductive physiology and behavior, possibly via separate actions on two forms of GnRH.

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“…How the photoperiodic changes in T 3 affect reproductive activity and body weight regulation remains to be established. Thyroid hormones are involved in the development and plasticity of the brain [45, 46, 71], and the local changes in T 3 have been suggested to trigger local morphological changes [54,72,73,74,75,76]. …”

Section: Photoperiodic Genes Define New Seasonal Loci In the Brainmentioning

confidence: 99%

Melatonin Controls Seasonal Breeding by a Network of Hypothalamic Targets

et al. 2009

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In seasonal species, the photoperiod (i.e. day length) tightly regulates reproduction to ensure that birth occurs at the most favourable time of year. In mammals, a distinct photoneuroendocrine circuit controls this process via the pineal hormone melatonin. This hormone is responsible for the seasonal timing of reproduction, but the anatomical substrates and the cellular mechanisms through which melatonin modulates seasonal functions remain imprecise. Recently, several genes have been identified as being regulated by the photoperiod in the brain of seasonal mammals. These genes are thought to play active roles in the regulation of seasonal biology, notably for the adjustment of reproduction and body weight. Here, we briefly review findings associated with the control of seasonal breeding and describe recent data ascribing photoperiodic roles to type 2 and type 3 deiodinases, to the Kiss1/GPR54 system and to the RFamide-related peptides.Interestingly, these systems involve different hypothalamic nuclei, suggesting that several brain loci may be crucial for melatonin to regulate reproduction, and thus represent key starting points to identify the long-sought-after mode and site(s) of action of melatonin. Such findings raise great hopes for the future and could herald a new era of research in the field of seasonal biology.

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Seasonal Morphological Changes in the Neuro-Glial Interaction between Gonadotropin-Releasing Hormone Nerve Terminals and Glial Endfeet in Japanese Quail

Cited by 185 publications

References 21 publications

Maternal photoperiod programs hypothalamic thyroid status via the fetal pituitary gland

Maternal photoperiod programs hypothalamic thyroid status via the fetal pituitary gland

Rapid inhibition of female sexual behavior by gonadotropin-inhibitory hormone (GnIH)

Melatonin Controls Seasonal Breeding by a Network of Hypothalamic Targets

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