Luteinizing hormone-releasing hormone (LHRH) neurons: Mechanism of pulsatile LHRH release

E, Terasawa

doi:10.1016/s0083-6729(01)63004-8

Cited by 81 publications

(44 citation statements)

References 217 publications

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“…Hypothalamic neuroendocrine cells are coupled (328,329,532) by Cx36, the only connexin which has so far been convincingly shown to be expressed at neuronal gap junction plaques (373,419). Electrophysiological studies testing gap junction blockers have indicated that this coupling is implicated in the control of the pulsatile release of several neuropeptides, including growth hormone releasing hormone (486), gonadotropin releasing hormone (553), and luteinizing hormone releasing hormone (535). Eventually, the endocrine cell types that form the anterior pituitary are coupled (137,305,359) via channels made predominantly of Cx43 and Cx26 (341,580).…”

Section: Peptide-producing Endocrinesmentioning

confidence: 99%

Connexins: Key Mediators of Endocrine Function

Bosco

Haefliger

Meda

2011

Physiological Reviews

158

185

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The appearance of multicellular organisms imposed the development of several mechanisms for cell-to-cell communication, whereby different types of cells coordinate their function. Some of these mechanisms depend on the intercellular diffusion of signal molecules in the extracellular spaces, whereas others require cell-to-cell contact. Among the latter mechanisms, those provided by the proteins of the connexin family are widespread in most tissues. Connexin signaling is achieved via direct exchanges of cytosolic molecules between adjacent cells at gap junctions, for cell-to-cell coupling, and possibly also involves the formation of membrane “hemi-channels,” for the extracellular release of cytosolic signals, direct interactions between connexins and other cell proteins, and coordinated influence on the expression of multiple genes. Connexin signaling appears to be an obligatory attribute of all multicellular exocrine and endocrine glands. Specifically, the experimental evidence we review here points to a direct participation of the Cx36 isoform in the function of the insulin-producing β-cells of the endocrine pancreas, and of the Cx40 isoform in the function of the renin-producing juxtaglomerular epithelioid cells of the kidney cortex.

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Section: Peptide-producing Endocrinesmentioning

confidence: 99%

Connexins: Key Mediators of Endocrine Function

Bosco

Haefliger

Meda

2011

Physiological Reviews

158

185

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“…These effects involve a negative (inhibitory) feedback control of GnRH and the pituitary gonadotrophins which is very potent in the immature individual (Grumbach and Styne, 2003). In the mature female, a so-called positive (stimulating) feedback is also exerted by E2 and leads to the preovulatory GnRH and gonadotrophin (FSH and LH) surge (Levine, 1997;Terasawa, 2001). E2 has been usually administered postnatally starting either at birth or by PND 5-12, i.e.…”

Section: E2 a Reference Natural Estrogenmentioning

confidence: 99%

Female sexual maturation and reproduction after prepubertal exposure to estrogens and endocrine disrupting chemicals: A review of rodent and human data

Rasier

Toppari

Parent

et al. 2006

Molecular and Cellular Endocrinology

145

108

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Natural hormones and some synthetic chemicals spread into our surrounding environment share the capacity to interact with hormone action and metabolism. Exposure to such compounds can cause a variety of developmental and reproductive detrimental abnormalities in wildlife species and, potentially, in human. Many experimental and epidemiological data have reported that exposure of the developing fetus or neonate to environmentally relevant concentrations of some among these endocrine disrupters induces morphological, biochemical and/or physiological disorders in brain and reproductive organs, by interfering with the hormone actions. The impact of such exposures on the hypothalamic-pituitary-gonadal axis and subsequent sexual maturation is the subject of the present review. We will highlight epidemiological human studies and the effects of early exposure during gestational, perinatal or postnatal life in female rodents.

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“…In adult rodents, GnRH is released from the median eminence at a frequency of about one pulse every 30 min. A slightly slower frequency of release (approximately 50 -60 min intervals) is observed in primates (Terasawa 2001, Gore et al 2004. The pulsatile pattern of GnRH (or LH) release is superimposed upon longer cycles of release, such as menstrual (primates) or estrous (rat, mouse, sheep) cycles.…”

Section: Gnrh Release and Agingmentioning

confidence: 99%

“…During aging, all of the parameters of pulsatile release (basal and mean concentrations, and pulse frequency) and the preovulatory surge are altered (as described below and summarized in Table 2). As all of these biologic rhythms are critical for normal reproductive function (Levine 1997, Terasawa 2001, age-related changes in these patterns may underlie the transition to acyclicity. To follow is a summary of in vivo and in vitro studies on GnRH or LH release in aging females.…”

Section: Gnrh Release and Agingmentioning

confidence: 99%

Neuroendocrine control of reproductive aging: roles of GnRH neurons

Yin

Gore²

2006

Reproduction

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The process of reproductive senescence in many female mammals, including humans, is characterized by a gradual transition from regular reproductive cycles to irregular cycles to eventual acyclicity, and ultimately a loss of fertility. In the present review, the role of the hypothalamic gonadotropin-releasing hormone (GnRH) neurons is considered in this context. GnRH neurons provide the primary driving force upon the other levels of the reproductive axis. With respect to aging, GnRH cells undergo changes in biosynthesis, processing and release of the GnRH decapeptide. GnRH neurons also exhibit morphologic and ultrastructural alterations that appear to underlie these biosynthetic properties. Thus, functional and morphologic changes in the GnRH neurosecretory system may play causal roles in the transition to acyclicity. In addition, GnRH neurons are regulated by numerous inputs from neurotransmitters, neuromodulators and glia. The relationship among GnRH cells and their inputs at the cell body (thereby affecting GnRH biosynthesis) and the neuroterminal (thereby affecting GnRH neurosecretion) is crucial to the function of the GnRH system, with age-related changes in these relationships contributing to the reproductive senescent process. Therefore, the aging hypothalamus is characterized by changes intrinsic to the GnRH cell, as well as its regulatory inputs, which summate to contribute to a loss of reproductive competence in aging females. Reproduction (2006) 131 403-414

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Luteinizing hormone-releasing hormone (LHRH) neurons: Mechanism of pulsatile LHRH release

Cited by 81 publications

References 217 publications

Connexins: Key Mediators of Endocrine Function

Connexins: Key Mediators of Endocrine Function

Female sexual maturation and reproduction after prepubertal exposure to estrogens and endocrine disrupting chemicals: A review of rodent and human data

Neuroendocrine control of reproductive aging: roles of GnRH neurons

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