Abstract:
:Increases in the level of cAMP stimulate the secretion of GnRH from GT1 GnRH neuronal cells. We hypothesized that cyclic nucleotide phosphodiesterases (PDEs), the enzymes that hydrolyze cAMP, may constitute a negative feedback signaling mechanism for GnRH regulation by decreasing the level of cAMP. GT1 cells were shown to express three PDEs by RT-PCR analysis: the cAMP-specific PDE4B and PDE4D and the calmodulin-dependent PDE1B. A splice variant of PDE4D, PDE4D3, which is activated when phosphorylated by cAMP-dependent protein kinase (PKA), was identified in GT1 cells by Western analysis. Consistent with PDEs negatively regulating GnRH secretion, treatment with the nonselective PDE inhibitor, IBMX, stimulated GnRH secretion 137% in 30-min static cultures. Furthermore, treatment with the PDE4-specific inhibitors Rolipram and RS-25344 increased GnRH secretion 48 and 125%, while treatment with the PDE1-specific inhibitor 8-MeoM-IBMX only caused a modest increase of 28%. In perifusion studies a rapid multi-fold stimulation of GnRH secretion was observed following treatment with IBMX, Rolipram or RS-25344. In conclusion, the level of PDE activity appears to be an important negative feedback signal for GnRH secretion. We hypothesize that activation of PDE4D3 by PKA may constitute a negative feedback signaling pathway which participates in the regulation of cAMP levels.
journal_name
Neuroendocrinologyjournal_title
Neuroendocrinologyauthors
Sakakibara H,Conti M,Weiner RIdoi
10.1159/000054386subject
Has Abstractpub_date
1998-12-01 00:00:00pages
365-73issue
6eissn
0028-3835issn
1423-0194pii
nen68365journal_volume
68pub_type
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journal_title:Neuroendocrinology
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更新日期:1988-07-01 00:00:00
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更新日期:1987-08-01 00:00:00
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更新日期:2020-01-01 00:00:00
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journal_title:Neuroendocrinology
pub_type: 杂志文章
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更新日期:2014-01-01 00:00:00
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