Function-related structural plasticity of the GnRH system

Prévot, Vincent; Hanchate, Naresh K.; Bellefontaine, Nicole; Sharif, Ariane; Parkash, Jyoti; Estrella, Cecilia; Allet, Cécile; Seranno, Sandrine De; Campagne, Céline; Tassigny, Xavier d’Anglemont de; Baroncini, Marc

doi:10.1016/j.yfrne.2010.05.003

Cited by 62 publications

(34 citation statements)

References 236 publications

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“…It consists of tanycytes, bipolar cells that are thought to derive from radial glial cells, but express distinct morphologic and molecular characteristics (59). Tanycytes have cell bodies lining the ventricle and long processes arching to the median eminence with end feet terminating on the fenestrated capillaries of the pituitary portal circulation (60).…”

Section: Discussionmentioning

confidence: 99%

Chronic Oestradiol Reduces the Dendritic Spine Density of KNDy (Kisspeptin/Neurokinin B/Dynorphin) Neurones in the Arcuate Nucleus of Ovariectomised Tac2‐Enhanced Green Fluorescent Protein Transgenic Mice

Cholanian

Krajewski-Hall

McMullen

et al. 2015

J Neuroendocrinology

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Neurones in the arcuate nucleus that express neurokinin B (NKB), kisspeptin and dynorphin (KNDy) play an important role in the reproductive axis. Oestradiol modulates the gene expression and somatic size of these neurones but there is limited information whether their dendritic structure, a correlate of cellular plasticity, is altered by oestrogens. Here we study the morphology of KNDy neurones by filling fluorescent neurones in the arcuate nucleus of Tac2-EGFP transgenic mice with biocytin. Filled neurones from ovariectomized (OVX) or OVX plus 17β-oestradiol (E2)-treated mice were visualized with anti-biotin immunohistochemistry and reconstructed in three dimensions with computer-assisted microscopy. KNDy neurones exhibited two primary dendrites, each with a few branches confined to the arcuate nucleus. Quantitative analysis revealed that E2 treatment of OVX mice decreased the cell size and dendritic spine density of KNDy neurones. The axons of KNDy neurones originated from the cell body or proximal dendrite and gave rise to local branches that appeared to terminate within the arcuate nucleus. Numerous terminal boutons were also visualized within the ependymal layer of the third ventricle adjacent to the arcuate nucleus. Axonal branches also projected to the adjacent median eminence and exited the arcuate nucleus. Confocal microscopy revealed close apposition of EGFP and GnRH-immunoreactive fibers within the median eminence and confirmed the presence of KNDy axon terminals in the ependymal layer of the third ventricle. The axonal branching pattern of KNDy neurones suggests that a single KNDy neurone could influence multiple arcuate neurones, tanycytes in the wall of the third ventricle, axon terminals in the median eminence and numerous areas outside of the arcuate nucleus. In parallel with its inhibitory effects on electrical excitability, E2 treatment of OVX Tac2-EGFP mice induces structural changes in the somata and dendrites of KNDy neurones.

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Section: Discussionmentioning

confidence: 99%

Chronic Oestradiol Reduces the Dendritic Spine Density of KNDy (Kisspeptin/Neurokinin B/Dynorphin) Neurones in the Arcuate Nucleus of Ovariectomised Tac2‐Enhanced Green Fluorescent Protein Transgenic Mice

Cholanian

Krajewski-Hall

McMullen

et al. 2015

J Neuroendocrinology

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“…Although the surge is not regulated by a single neuronal population (40) and involves cells at the ME (46), kisspeptin is a powerful stimulator of GnRH neurons (47, 48) and direct inputs to GnRH neurons, via GPR54, is necessary (31). The RP3V neuronal subpopulation, larger in females and upregulated by estradiol (32), plays a critical role in the activation of GnRH neurons involved in the surge (49).…”

Section: Gnrh Secretion and Fertilitymentioning

confidence: 99%

Progress and Challenges in the Search for the Mechanisms of Pulsatile Gonadotropin-Releasing Hormone Secretion

Constantin

2017

Front. Endocrinol.

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Fertility relies on the proper functioning of the hypothalamic–pituitary–gonadal axis. The hormonal cascade begins with hypothalamic neurons secreting gonadotropin-releasing hormone (GnRH) into the hypophyseal portal system. In turn, the GnRH-activated gonadotrophs in the anterior pituitary release gonadotropins, which then act on the gonads to regulate gametogenesis and sex steroidogenesis. Finally, sex steroids close this axis by feeding back to the hypothalamus. Despite this seeming straightforwardness, the axis is orchestrated by a complex neuronal network in the central nervous system. For reproductive success, GnRH neurons, the final output of this network, must integrate and translate a wide range of cues, both environmental and physiological, to the gonadotrophs via pulsatile GnRH secretion. This secretory profile is critical for gonadotropic function, yet the mechanisms underlying these pulses remain unknown. Literature supports both intrinsically and extrinsically driven GnRH neuronal activity. However, the caveat of the techniques supporting either one of the two hypotheses is the gap between events recorded at a single-cell level and GnRH secretion measured at the population level. This review aims to compile data about GnRH neuronal activity focusing on the physiological output, GnRH secretion.

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“…The median eminence, which lies ventrally to the third ventricle in the tuberal region of the hypothalamus, is increasingly recognized as a key site for GnRH release regulation [5,9,111,112]. Modulation of GnRH release by NO within the median eminence was suggested by early studies performed by McCann and colleagues.…”

Section: Endothelial Nitric Oxide Controls Gnrh Release At the Neurohmentioning

confidence: 99%

“…In parallel, estrogens stimulate eNOS expression in median eminence endothelial cells. Both tanycytes and endothelial cells were shown to express ERs in vitro [132] and in vivo [133] [adapted from [9], [150], with permission]. …”

Section: Endothelial Nitric Oxide Controls Gnrh Release At the Neurohmentioning

confidence: 99%

“…As the final common pathway for the central control of reproduction, gonadotropin-releasing hormone (GnRH) neurons are regulated by multiple neuronal networks and interactions with non-neuronal cells that intermingle in a complex array of transsynaptic inputs [1,2,3] and paracrine communication [4,5], subjected to the modulatory influence of gonadal steroids that prompts both chemical [6,7] and structural plasticity [8,9]. In rodents, the cell bodies of GnRH neuroendocrine neurons are mostly located in the preoptic region.…”

Section: Introductionmentioning

confidence: 99%

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Nitric Oxide as Key Mediator of Neuron-to-Neuron and Endothelia-to-Glia Communication Involved in the Neuroendocrine Control of Reproduction

Bellefontaine

Hanchate²,

Parkash³

et al. 2011

Neuroendocrinology

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Nitric oxide (NO) is a peculiar chemical transmitter that freely diffuses through aqueous and lipid environments and plays a role in major aspects of brain function. Within the hypothalamus, NO exerts critical effects upon the gonadotropin-releasing hormone (GnRH) network to maintain fertility. Here, we review recent evidence that NO regulates major aspects of the GnRH neuron physiology. Far more active than once thought, NO powerfully controls GnRH neuronal activity, GnRH release and structural plasticity at the neurohemal junction. In the preoptic region, neuronal nitric oxide synthase (nNOS) activity is tightly regulated by estrogens and is found to be maximal at the proestrus stage. Natural fluctuations of estrogens control both the differential coupling of this Ca²⁺-activated enzyme to glutamate N-methyl-D-aspartic acid receptor channels and phosphorylation-mediated nNOS activation. Furthermore, NO endogenously produced by neurons expressing nNOS acutely and directly suppresses spontaneous firing in GnRH neurons, which suggests that neuronal NO may serve as a synchronizing switch within the preoptic region. At the median eminence, NO is spontaneously released from an endothelial source and follows a pulsatile and cyclic pattern of secretion. Importantly, GnRH release appears to be causally related to endothelial NO release. NO is also highly involved in mediating the dialogue set in motion between vascular endothelial cells and tanycytes that control the direct access of GnRH neurons to the pituitary portal blood during the estrous cycle. Altogether, these data raise the intriguing possibility that the neuroendocrine brain uses NO to coordinate both GnRH neuronal activity and GnRH release at key stages of reproductive physiology.

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Function-related structural plasticity of the GnRH system

Cited by 62 publications

References 236 publications

Chronic Oestradiol Reduces the Dendritic Spine Density of KNDy (Kisspeptin/Neurokinin B/Dynorphin) Neurones in the Arcuate Nucleus of Ovariectomised Tac2‐Enhanced Green Fluorescent Protein Transgenic Mice

Chronic Oestradiol Reduces the Dendritic Spine Density of KNDy (Kisspeptin/Neurokinin B/Dynorphin) Neurones in the Arcuate Nucleus of Ovariectomised Tac2‐Enhanced Green Fluorescent Protein Transgenic Mice

Progress and Challenges in the Search for the Mechanisms of Pulsatile Gonadotropin-Releasing Hormone Secretion

Nitric Oxide as Key Mediator of Neuron-to-Neuron and Endothelia-to-Glia Communication Involved in the Neuroendocrine Control of Reproduction

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