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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Is GnRH suppression hurting us?
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<blockquote data-quote="Cataceous" data-source="post: 237112" data-attributes="member: 38109"><p>Here's a study looking at an apparent protective effect of GnRH in rats, which acts via enhancing estradiol in the hippocampus. If I'm interpreting this correctly, they're saying that the effect is not via regulation of estradiol synthesis, because "Letrozole did not reverse GnRH modulatory effects on hippocampal E2 levels and neuroprotection."</p><p></p><p style="margin-left: 20px"><strong><em>Introduction: </em></strong><em>The 17β-estradiol (E2) enhances hippocampal dendritic spine synapses, facilitates learning processes, and exerts neuroprotection. Brain estrogen decline has been reported in Alzheimer's disease. The role of GnRH in modulating steroid biosynthesis convinced us <strong>to examine whether hippocampal GnRH administration could enhance the local E2 levels and overcome the development of cognition decline in amyloid β (Aβ) neurotoxicity</strong>. To explore if GnRH acts through regulating E2 synthesis, letrozole, an aromatase inhibitor, has been applied in combination with GnRH.</em></p> <p style="margin-left: 20px"></p> <p style="margin-left: 20px"><em><strong>Methods: </strong>Female rats received an intracerebroventricular injection of Aβ. The GnRH and, or letrozole were injected into the CA1 for 14 consecutive days. Working memory, novel object recognition memory, and anxiety-like behavior were evaluated. Serum and hippocampal E2 levels were measured. Hippocampal mRNA expression of GnRH (GnRH-R) and E2 (ERα and ERβ) receptors was assessed. GnRH effect on the excitability of pyramidal cells was studied by in vivo single-unit recording.</em></p> <p style="margin-left: 20px"></p> <p style="margin-left: 20px"><em><strong>Results: GnRH increased hippocampal E2 levels</strong>, evoked an increase in the spontaneous firing of pyramidal neurons, and caused mRNA overexpression of hippocampal GnRH receptors. <strong>GnRH prevented the adverse effects of Aβ on working memory, NOR index, and anxiogenic behavior. Letrozole did not reverse GnRH modulatory effects on hippocampal E2 levels and neuroprotection</strong>.</em></p> <p style="margin-left: 20px"></p> <p style="margin-left: 20px"><em><strong>Conclusion: GnRH prevented the Aβ-induced memory deficit, which may be mediated through hippocampal E2 levels enhancement.</strong> The electrophysiological analysis revealed the enhanced neuronal excitability in the CA1 region. All these data suggest that GnRH might be a promising candidate that reduces anxiety and improves memory indices in the context of Aβ neurotoxicity.</em></p><p></p><p>[URL unfurl="true"]https://pubmed.ncbi.nlm.nih.gov/32805333/[/URL]</p></blockquote><p></p>
[QUOTE="Cataceous, post: 237112, member: 38109"] Here's a study looking at an apparent protective effect of GnRH in rats, which acts via enhancing estradiol in the hippocampus. If I'm interpreting this correctly, they're saying that the effect is not via regulation of estradiol synthesis, because "Letrozole did not reverse GnRH modulatory effects on hippocampal E2 levels and neuroprotection." [INDENT][B][I]Introduction: [/I][/B][I]The 17β-estradiol (E2) enhances hippocampal dendritic spine synapses, facilitates learning processes, and exerts neuroprotection. Brain estrogen decline has been reported in Alzheimer's disease. The role of GnRH in modulating steroid biosynthesis convinced us [B]to examine whether hippocampal GnRH administration could enhance the local E2 levels and overcome the development of cognition decline in amyloid β (Aβ) neurotoxicity[/B]. To explore if GnRH acts through regulating E2 synthesis, letrozole, an aromatase inhibitor, has been applied in combination with GnRH.[/I][/INDENT] [INDENT][/INDENT] [INDENT][I][B]Methods: [/B]Female rats received an intracerebroventricular injection of Aβ. The GnRH and, or letrozole were injected into the CA1 for 14 consecutive days. Working memory, novel object recognition memory, and anxiety-like behavior were evaluated. Serum and hippocampal E2 levels were measured. Hippocampal mRNA expression of GnRH (GnRH-R) and E2 (ERα and ERβ) receptors was assessed. GnRH effect on the excitability of pyramidal cells was studied by in vivo single-unit recording.[/I][/INDENT] [INDENT][/INDENT] [INDENT][I][B]Results: GnRH increased hippocampal E2 levels[/B], evoked an increase in the spontaneous firing of pyramidal neurons, and caused mRNA overexpression of hippocampal GnRH receptors. [B]GnRH prevented the adverse effects of Aβ on working memory, NOR index, and anxiogenic behavior. Letrozole did not reverse GnRH modulatory effects on hippocampal E2 levels and neuroprotection[/B].[/I][/INDENT] [INDENT][/INDENT] [INDENT][I][B]Conclusion: GnRH prevented the Aβ-induced memory deficit, which may be mediated through hippocampal E2 levels enhancement.[/B] The electrophysiological analysis revealed the enhanced neuronal excitability in the CA1 region. All these data suggest that GnRH might be a promising candidate that reduces anxiety and improves memory indices in the context of Aβ neurotoxicity.[/I][/INDENT] [URL unfurl="true"]https://pubmed.ncbi.nlm.nih.gov/32805333/[/URL] [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Is GnRH suppression hurting us?
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