ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Kisspeptin depolarizes gonadotropin-releasing hormone neurons through activation of TRPC-like cationic channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 2 of them syntheses that pooled it.
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Who cites it
124 citing papers in PubMed, 2 syntheses or guidelines pooled it, 234 citations in OpenAlex.
- Pooled it
- Kisspeptins in human reproduction-future therapeutic potential.Journal of assisted reproduction and genetics · 2012Pooled it
- Kisspeptin System: A Modulator of Neuroinflammation and Behaviour in Temporal Lobe Epileptic Rats.Molecular neurobiology · 2026Article
- Reproduction under Siege: How Chronic Stress Hijacks the HPG Axis?Neuroendocrinology · 2026Review
- Article
- Altered Electrophysiology and Transcriptome of GnRH Neurons in Middle-Aged Female Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Nonsteroidal Anti-Inflammatory Drugs as Modulators of Cation Channels: Fenamates Repurposing in Channelopathies.ChemMedChem · 2025Review
- Sexually dimorphic distribution of Kiss1 neurons in the bed nucleus of the stria terminalis.Journal of neuroendocrinology · 2025Article
- The role of neonatal kisspeptin in long-term social behavior in mammals.Communications biology · 2025Article
- Comprehensive chemoanatomical mapping, and the gonadal regulation, of seven kisspeptin neuronal populations in the mouse brain.Journal of neuroendocrinology · 2025Article
- Canonical transient receptor potential channels and hypothalamic control of homeostatic functions.Journal of neuroendocrinology · 2024Review
- Kisspeptin a potential therapeutic target in treatment of both metabolic and reproductive dysfunction.Journal of diabetes · 2024Review
- Gonadal Feedback Alters the Relationship between Action Potentials and Hormone Release in Gonadotropin-Releasing Hormone Neurons in Male Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Mechanisms linking neurological disorders with reproductive endocrine dysfunction: Insights from epilepsy research.Frontiers in neuroendocrinology · 2023Review
- Hypothalamic kisspeptin neurons as potential mediators of estradiol negative and positive feedback.Peptides · 2023Review
- Modelling KNDy neurons and gonadotropin-releasing hormone pulse generation.Current opinion in endocrine and metabolic research · 2022Review
- Increased GABA transmission to GnRH neurons after intrahippocampal kainic acid injection in mice is sex-specific and associated with estrous cycle disruption.Neurobiology of disease · 2022Article
- The E3 ubiquitin ligase RNF216/TRIAD3 is a key coordinator of the hypothalamic-pituitary-gonadal axis.iScience · 2022Article
- Estrogenic regulation of reproduction and energy homeostasis by a triumvirate of hypothalamic arcuate neurons.Journal of neuroendocrinology · 2022Review
- The electrophysiologic properties of gonadotropin-releasing hormone neurons.Journal of neuroendocrinology · 2022Review
64 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Kisspeptin and its cognate receptor, GPR54, are critical for reproductive development and for the regulation of gonadotropin-releasing hormone (GnRH) secretion. Although kisspeptin has been found to depolarize GnRH neurons, the underlying ionic mechanism has not been elucidated. Presently, we found that kisspeptin depolarized GnRH neurons in a concentration-dependent manner with a maximum depolarization of 22.6 +/- 0.6 mV and EC(50) of 2.8 +/- 0.2 nM. Under voltage-clamp conditions, kisspeptin induced an inward current of 18.2 +/- 1.6 pA (V(hold) = -60 mV) that reversed near -115 mV in GnRH neurons. The more negative reversal potential than E(K)(+) (-90 mV) was caused by the concurrent inhibition of barium-sensitive, inwardly rectifying (Kir) potassium channels and activation of sodium-dependent, nonselective cationic channels (NSCCs). Indeed, reducing extracellular Na(+) (to 5 mM) essentially eliminated the kisspeptin-induced inward current. The current-voltage relationships of the kisspeptin-activated NSCC currents exhibited double rectification with negative slope conductance below -40 mV in the majority of the cells. Pharmacological examination showed that the kisspeptin-induced inward currents were blocked by TRPC (canonical transient receptor potential) channel blockers 2-APB (2-aminoethyl diphenylborinate), flufenamic acid, SKF96365 (1-[beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl]-1H-imidazole hydrochloride), and Cd(2+), but not by lanthanum (100 microM). Furthermore, single-cell reverse transcription-PCR analysis revealed that TRPC1, TRPC3, TRPC4, TRPC5, TRPC6, and TRPC7 subunits were expressed in GnRH neurons. Therefore, it appears that kisspeptin depolarizes GnRH neurons through activating TRPC-like channels and, to a lesser extent, inhibition of Kir channels. These actions of kisspeptin contribute to the pronounced excitation of GnRH neurons that is critical for mammalian reproduction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.