These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Partial characterization of K(+)-induced increase in [Ca2+]cyt and GnRH release in GT1-7 neurons.
    Author: Javors MA, King TS, Chang X, Klein NA, Schenken RS.
    Journal: Brain Res; 1995 Oct 02; 694(1-2):49-54. PubMed ID: 8974663.
    Abstract:
    Secretion of pituitary gonadotropins is regulated centrally by the hypothalamic decapeptide gonadotropin releasing hormone (GnRH). Using the immortalized hypothalamic GT1-7 neuron, we characterized pharmacologically the dynamics of cytosolic Ca2+ and GnRH release in response to K+-induced depolarization of GT1-7 neurons. Our results showed that K+ concentrations from 7.5 to 60 mM increased [Ca2+]cyt in a concentration-dependent manner. Resting [Ca2+]cyt in GT1 -7 cells was determined to be 69.7 +/- 4.0 nM (mean +/- S.E.M.; n = 69). K+-induced increases in [Ca2+]cyt ranged from 58.2 nM at 7.5 mM [K+] to 347 nM at 60 mM [K+]. K+-induced GnRH release ranged from about 10 pg/ml at 7.5 mM [K+] to about 60 pg/ml at 45 mM [K+]. K+-induced increases in (Ca2+]cyt and GnRH release were enhanced by 1 microM BayK 8644, an L-type Ca2+ channel agonist. The BayK enhancement was completely inhibited by 1 microM nimodipine, an L-type Ca2+ channel antagonist. Nimodipine (1 microM) alone partially inhibited K+-induced increases in [Ca2+]cyt and GnRH release. Conotoxin (1 microM) alone had no effect on K+-induced GnRH release or [Ca2+]cyt, but the combination of conotoxin (1 microM) and nimodipine (1 microM) inhibited K+-induced increase in [Ca2+]cyt significantly more (p < 0.02) than nimodipine alone, suggesting that N-type Ca2+ channels exist in GT1-7 neurons and may be part of the response to K+. The response of [Ca2+]cyt to K+ was linear with increasing [K+] whereas the response of GnRH release to increasing [K+] appeared to be saturable. K+-induced increase in [Ca2+]cyt and GnRH release required extracellular [Ca2+]. These experiments suggest that voltage dependent N- and L-type Ca2+ channels are present in immortalized GT1-7 neurons and that GnRH release is, at least in part, dependent on these channels for release of GnRH.
    [Abstract] [Full Text] [Related] [New Search]