English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Gamma-aminobutyric acid (GABA) is one of the most important neurotransmitters that regulate the excitability of GnRH neurons. Numerous studies have shown that GABA activates Cl(-) currents in GnRH neurons, and these effects are antagonized by GABA(A) receptor antagonists. The GABA(B) receptor is a heterodimer composed of GABA(B) R1 and R2, and although both subunits have been localized in GnRH neurons, nothing is known about the cellular signaling of this G alpha(i,o)-coupled receptor in GnRH neurons. Using whole-cell recordings from mouse enhanced green fluorescent protein-GnRH neurons, we found that the GABA(B) receptor agonist baclofen hyperpolarized GnRH neurons through activation of an inwardly rectifying K(+) current in a concentration-dependent manner. The effects of baclofen were antagonized by the selective GABA(B) receptor antagonist CGP 52432 with a K(i) (inhibitory constant) of 85 nm. Furthermore, in the presence of the GABA(A) receptor antagonist picrotoxin, GABA hyperpolarized GnRH neurons in a similar manner. Treatment with 17beta-estradiol as compared with oil vehicle did not significantly alter either the EC(50) for the baclofen-induced response (0.8 +/- 0.1 vs. 1.0 +/- 0.1 microM, respectively) or the maximal outward current (10.8 +/- 1.7 pA vs. 11.4 +/- 0.6 pA, respectively) in GnRH neurons. However, the outward current (and membrane hyperpolarization) was abrogated by submaximal concentrations of the G protein-coupled receptor 54 (GPR54) agonist kisspeptin-10 in both groups, indicating that G alpha(q)-coupled (GPR54) can desensitize the GABA(B) receptor-mediated response. Therefore, the activation of GABA(B) receptors in GnRH neurons may provide increased inhibitory tone during estrogen-negative feedback states that is attenuated by kisspeptin during positive feedback.

endocrinology

γ-Aminobutyric Acid B Receptor Mediated Inhibition of Gonadotropin-Releasing Hormone Neurons Is Suppressed by Kisspeptin-G Protein-Coupled Receptor 54 Signaling