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Testosterone Replacement, Low T, HCG, & Beyond
Clomid for PCT, fertility or low T
A fresh look at kisspeptin neuron synchronization
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<blockquote data-quote="madman" data-source="post: 243307" data-attributes="member: 13851"><p><strong>Mechanism of kisspeptin neuron synchronization for pulsatile hormone secretion in male mice (2023)</strong></p><p><em>Su Young Han, Paul G. Morris, Jae-Chang Kim, ..., Shel-Hwa Yeo, H. James McQuillan, Allan E. Herbison</em></p><p><em></em></p><p><em></em></p><p><em>[ATTACH=full]28456[/ATTACH]</em></p><p></p><p></p><p><strong>SUMMARY</strong></p><p></p><p><em>The mechanism by which arcuate nucleus kisspeptin (ARNKISS) neurons co-expressing glutamate, neurokinin B, and dynorphin intermittently synchronize their activity to generate pulsatile hormone secretion remains unknown. <strong>An acute brain slice preparation maintaining synchronized ARNKISS neuron burst firing was used alongside in vivo GCaMP GRIN lens microendoscope and fiber photometry imaging coupled with intraARN microinfusion. Studies in intact and gonadectomized male mice revealed that ARNKISS neuron synchronizations result from near-random emergent network activity within the population and that this was critically dependent on local glutamate-AMPA signaling. <u>Whereas neurokinin B operated to potentiate glutamate-generated synchronizations, dynorphin-kappa opioid tone within the network served as a gate for synchronization initiation</u>.</strong> These observations force a departure from the existing ‘‘KNDy hypothesis’’ for ARNKISS neuron synchronization. <strong>A ‘‘<u>glutamate two-transition</u>’’ mechanism is proposed to underlie synchronizations in this key hypothalamic central pattern generator driving mammalian fertility.</strong></em></p><p></p><p></p><p></p><p></p><p><strong>Limitations of the study </strong></p><p></p><p><em>A key limitation of the current study and proposed ‘‘glutamate two-transition’’ model is that the work has been undertaken in male mice. Although it is thought that pulse generator operation is fundamentally the same in males and females,4 it remains that future studies will need to ensure that the same mechanism operates in females. Equally, it will be important to evaluate whether the mechanism delineated here for mice is applicable to other species. Although there are rather few studies using the intra-ARN administration of receptor antagonists in relation to the pulse generator, results from the rat40 are very similar to those reported here for the mouse, while data from sheep41 differ in some respects.</em></p><p></p><p><strong><em>In summary, we demonstrate here the key features of the synchronization mechanism used by the central pattern generator controlling GnRH secretion in male mice. We propose a substantial departure from the existing ‘‘KNDy hypothesis’’ with glutamate as the primary transmitter generating synchronization within the network and neuropeptides as neuromodulators; dynorphin in state-dependent synchronization initiation and NKB operating to potentiate the magnitude of synchronizations (Figure 7). <u>Kisspeptin itself does not contribute to the synchronization mechanism but is used as the exclusive output signal to the GnRH neuron</u>.56 It is expected that an accurate definition of GnRH pulse generator operation will be beneficial to the treatment of infertility in the clinic.</em></strong></p><p></p><p></p><p>[ATTACH=full]28455[/ATTACH]</p><p><strong>Figure 7. ‘‘<u>Glutamate two-transition</u>’’ model for ARNKISS neuron synchronization Stochastic, glutamate-dependent coupling between overlapping small groups of ARNKISS neurons (different colors) generates ongoing miniature synchronization episodes (mSEs). The first transition involves the emergence of a widespread population synchronization event (SE, pink) through exponential glutamate-driven self-excitation. The efficiency of this transition is modulated by dynorphin-kappa opioid tone within the network and also afferent inputs to the pulse generator that regulate its frequency of activity. The second transition involves the potentiation of already established synchronous activity by NKB increasing both the number of ARNKISS neurons involved in an SE and their individual levels of excitation. Intrinsic mechanisms are then likely involved in synchronization termination.</strong></p></blockquote><p></p>
[QUOTE="madman, post: 243307, member: 13851"] [B]Mechanism of kisspeptin neuron synchronization for pulsatile hormone secretion in male mice (2023)[/B] [I]Su Young Han, Paul G. Morris, Jae-Chang Kim, ..., Shel-Hwa Yeo, H. James McQuillan, Allan E. Herbison [ATTACH type="full" alt="Screenshot (19974).png"]28456[/ATTACH][/I] [B]SUMMARY[/B] [I]The mechanism by which arcuate nucleus kisspeptin (ARNKISS) neurons co-expressing glutamate, neurokinin B, and dynorphin intermittently synchronize their activity to generate pulsatile hormone secretion remains unknown. [B]An acute brain slice preparation maintaining synchronized ARNKISS neuron burst firing was used alongside in vivo GCaMP GRIN lens microendoscope and fiber photometry imaging coupled with intraARN microinfusion. Studies in intact and gonadectomized male mice revealed that ARNKISS neuron synchronizations result from near-random emergent network activity within the population and that this was critically dependent on local glutamate-AMPA signaling. [U]Whereas neurokinin B operated to potentiate glutamate-generated synchronizations, dynorphin-kappa opioid tone within the network served as a gate for synchronization initiation[/U].[/B] These observations force a departure from the existing ‘‘KNDy hypothesis’’ for ARNKISS neuron synchronization. [B]A ‘‘[U]glutamate two-transition[/U]’’ mechanism is proposed to underlie synchronizations in this key hypothalamic central pattern generator driving mammalian fertility.[/B][/I] [B]Limitations of the study [/B] [I]A key limitation of the current study and proposed ‘‘glutamate two-transition’’ model is that the work has been undertaken in male mice. Although it is thought that pulse generator operation is fundamentally the same in males and females,4 it remains that future studies will need to ensure that the same mechanism operates in females. Equally, it will be important to evaluate whether the mechanism delineated here for mice is applicable to other species. Although there are rather few studies using the intra-ARN administration of receptor antagonists in relation to the pulse generator, results from the rat40 are very similar to those reported here for the mouse, while data from sheep41 differ in some respects.[/I] [B][I]In summary, we demonstrate here the key features of the synchronization mechanism used by the central pattern generator controlling GnRH secretion in male mice. We propose a substantial departure from the existing ‘‘KNDy hypothesis’’ with glutamate as the primary transmitter generating synchronization within the network and neuropeptides as neuromodulators; dynorphin in state-dependent synchronization initiation and NKB operating to potentiate the magnitude of synchronizations (Figure 7). [U]Kisspeptin itself does not contribute to the synchronization mechanism but is used as the exclusive output signal to the GnRH neuron[/U].56 It is expected that an accurate definition of GnRH pulse generator operation will be beneficial to the treatment of infertility in the clinic.[/I][/B] [ATTACH type="full" alt="Screenshot (19975).png"]28455[/ATTACH] [B]Figure 7. ‘‘[U]Glutamate two-transition[/U]’’ model for ARNKISS neuron synchronization Stochastic, glutamate-dependent coupling between overlapping small groups of ARNKISS neurons (different colors) generates ongoing miniature synchronization episodes (mSEs). The first transition involves the emergence of a widespread population synchronization event (SE, pink) through exponential glutamate-driven self-excitation. The efficiency of this transition is modulated by dynorphin-kappa opioid tone within the network and also afferent inputs to the pulse generator that regulate its frequency of activity. The second transition involves the potentiation of already established synchronous activity by NKB increasing both the number of ARNKISS neurons involved in an SE and their individual levels of excitation. Intrinsic mechanisms are then likely involved in synchronization termination.[/B] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Clomid for PCT, fertility or low T
A fresh look at kisspeptin neuron synchronization
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