Kisspeptin depolarizes gonadotropin-releasing hormone neurons through activation of TRPC-like cationic channels.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
Chunguang ZhangOline K Rønnekleiv

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 (canonic...Continue Reading

Citations

Sep 28, 2012·Journal of Assisted Reproduction and Genetics·Kulvinder Kochar KaurMandeep Singh
Sep 8, 2010·Brain Research·Oline K RønnekleivChunguang Zhang
Oct 7, 2009·Proceedings of the National Academy of Sciences of the United States of America·Min WuMeenakshi Alreja
Sep 8, 2011·Proceedings of the National Academy of Sciences of the United States of America·Jerome ClasadonteVincent Prevot
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Aug 28, 2009·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Chunguang ZhangOline K Rønnekleiv
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