| http://purl.uniprot.org/citations/18535104 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18535104 | http://www.w3.org/2000/01/rdf-schema#comment | "GHRH depolarizes the membrane of somatotropes, leading to an increase in intracellular free Ca2+ concentration and GH secretion. Na+ channels mediate the rapid depolarization during the initial phase of the action potential, and this regulates Ca2+ influx and GH secretion. GHRH increases a tetrodotoxin-sensitive somatotrope Na+ current that is mediated by cAMP. TTX-resistant (TTX-R) Na+ channels are abundant in sensory neurons and cardiac myocytes, but their occurrence and/or function in somatotropes has not been investigated. Here we demonstrate expression of TTX-R Na+ channels and a TTX-R Na+ current, using patch-clamp method, in green fluorescent protein-GH transgenic mouse somatotropes. GHRH (100 nm) increased the TTX-R Na+ current in a reversible manner. The GHRH-induced increase in TTX-R Na+ current was not affected by the cAMP antagonist Rp-cAMP or protein kinase A inhibitors KT5720 or H89. The TTX-R current was increased by 8-bromoadenosine-cAMP (cAMP analog), forskolin (adenylyl-cyclase activator), and 3-isobutyl-1-methylxanthine (phosphodiesterase inhibitor), but the additional, GHRH-induced increase in TTX-R Na+ currents was not affected. U-73122 (phospholipase C inhibitor) and protein kinase C (PKC) inhibitors, Gö-6983 and chelerythrine, blocked the effect of GHRH. PKC activators, phorbol dibutyrate and phorbol myristate acetate, increased the TTX-R Na+ current, but GHRH had no further effect on the current. Na+-free extracellular medium significantly reduced GHRH-stimulated GH secretion. We conclude that GHRH-induced increase in the TTX-R Na+ current in mouse somatotropes is mediated by the PKC system. An increase in the TTX-R Na+ current may contribute to the GHRH-induced exocytosis of GH granules from mouse somatotropes."xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.org/dc/terms/identifier | "doi:10.1210/en.2008-0405"xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/author | "Chen C."xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/author | "Wang K."xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/author | "Yang S.K."xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/author | "Parkington H."xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/name | "Endocrinology"xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/pages | "4726-4735"xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/title | "Involvement of tetrodotoxin-resistant Na+ current and protein kinase C in the action of growth hormone (GH)-releasing hormone on primary cultured somatotropes from GH-green fluorescent protein transgenic mice."xsd:string |
| http://purl.uniprot.org/citations/18535104 | http://purl.uniprot.org/core/volume | "149"xsd:string |
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