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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
The KiNG of reproduction: kisspeptin/ nNOS interactions shaping hypothalamic GnRH release
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<blockquote data-quote="madman" data-source="post: 200848" data-attributes="member: 13851"><p><strong>Figure 3. Involvement of the KiNG network in shaping GnRH pulsatile and surge release. a) The KiNG network is part of the “GnRH pulse” and “GnRH surge” generators. Within the preoptic area (left panel), kisspeptin neurons (blue) and nNOS neurons communicate with the scattered GnRH neuronal cell bodies (green) located in the organum vasculosum laminae terminalis (OV) and the median preoptic nucleus (MePO). (1) Kisspeptin neurons of the anteroventral periventricular nucleus (AVPV) can both directly excite GnRH neurons (2) and promote the phosphorylation of nNOS in the OV/MePO, inducing its activation and subsequently NO production. Thereupon, NO may diffuse through volume transmission in the vicinity of GnRH neuronal cell bodies (3) acting as a brake to GnRH neurons, which may uphold their synchronous activity at the time of the preovulatory GnRH surge. Within the arcuate nucleus (ARH) (right panel) kisspeptin and nNOS neurons are in close proximity with the GnRH distal dendrites and terminals (green). (1) ARH kisspeptin neurons stimulate GnRH secretion; (2) concomitantly kisspeptin release may promote the activation of the nNOS population in the ARH. Production of NO in the vicinity of GnRH terminals (3) may inhibit GnRH neurons, contributing to the termination of GnRH/LH pulse. Considering ARH kisspeptin neurons can interact with the AVPV kisspeptin population we could also imagine that ARH kisspeptin neurons might indirectly interact with OV/MePO nNOS cells via their AVPV counterparts, hence promoting the action of NO at the level of GnRH neuronal soma.</strong></p><p><strong></strong></p><p><strong>(b) Proposed mode of action of the nNOS/ kisspeptin microcircuit during GnRH pulse. During the gonadal steroid hormone-mediated negative feedback, (1) ARH kisspeptin neurons activate the GPR54-expressing GnRH neurons promoting GnRH release. Kisspeptin also (2) acts on the GPR54-expressing nNOS neurons, promoting the activation of the nNOS enzyme triggering NO production. In turn, (3) NO acts on the GnRH neurons as the “OFF” signal necessary for GnRH neurons to return to their baseline activity; thus, enabling them to respond to forthcoming stimulus. This dynamic crosstalk driving depolarizing and hyperpolarizing responses in GnRH neurons (1, 2, 3) may give the pulse-like shape of the GnRH/LH release. Therefore, NO may operate as an important messenger for the estrogen-mediated switch from negative to positive feedback according to the sum of responses from the interaction between NO and kisspeptinergic signaling.</strong></p><p><strong>[ATTACH=full]14126[/ATTACH]</strong></p><p><strong>[ATTACH=full]14127[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 200848, member: 13851"] [B]Figure 3. Involvement of the KiNG network in shaping GnRH pulsatile and surge release. a) The KiNG network is part of the “GnRH pulse” and “GnRH surge” generators. Within the preoptic area (left panel), kisspeptin neurons (blue) and nNOS neurons communicate with the scattered GnRH neuronal cell bodies (green) located in the organum vasculosum laminae terminalis (OV) and the median preoptic nucleus (MePO). (1) Kisspeptin neurons of the anteroventral periventricular nucleus (AVPV) can both directly excite GnRH neurons (2) and promote the phosphorylation of nNOS in the OV/MePO, inducing its activation and subsequently NO production. Thereupon, NO may diffuse through volume transmission in the vicinity of GnRH neuronal cell bodies (3) acting as a brake to GnRH neurons, which may uphold their synchronous activity at the time of the preovulatory GnRH surge. Within the arcuate nucleus (ARH) (right panel) kisspeptin and nNOS neurons are in close proximity with the GnRH distal dendrites and terminals (green). (1) ARH kisspeptin neurons stimulate GnRH secretion; (2) concomitantly kisspeptin release may promote the activation of the nNOS population in the ARH. Production of NO in the vicinity of GnRH terminals (3) may inhibit GnRH neurons, contributing to the termination of GnRH/LH pulse. Considering ARH kisspeptin neurons can interact with the AVPV kisspeptin population we could also imagine that ARH kisspeptin neurons might indirectly interact with OV/MePO nNOS cells via their AVPV counterparts, hence promoting the action of NO at the level of GnRH neuronal soma. (b) Proposed mode of action of the nNOS/ kisspeptin microcircuit during GnRH pulse. During the gonadal steroid hormone-mediated negative feedback, (1) ARH kisspeptin neurons activate the GPR54-expressing GnRH neurons promoting GnRH release. Kisspeptin also (2) acts on the GPR54-expressing nNOS neurons, promoting the activation of the nNOS enzyme triggering NO production. In turn, (3) NO acts on the GnRH neurons as the “OFF” signal necessary for GnRH neurons to return to their baseline activity; thus, enabling them to respond to forthcoming stimulus. This dynamic crosstalk driving depolarizing and hyperpolarizing responses in GnRH neurons (1, 2, 3) may give the pulse-like shape of the GnRH/LH release. Therefore, NO may operate as an important messenger for the estrogen-mediated switch from negative to positive feedback according to the sum of responses from the interaction between NO and kisspeptinergic signaling. [ATTACH type="full"]14126[/ATTACH] [ATTACH type="full"]14127[/ATTACH][/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone and Men's Health Articles
The KiNG of reproduction: kisspeptin/ nNOS interactions shaping hypothalamic GnRH release
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