Changes in Hormone Sensitivity of the Adenylate Cyclase Signaling System in the Testicular Tissue of Rats with Neonatal Streptozotocin-Induced Diabetes

2009 ◽  
Vol 148 (3) ◽  
pp. 394-398 ◽  
Author(s):  
A. O. Shpakov ◽  
K. V. Derkach ◽  
V. M. Bondareva
Keyword(s):  
Adenylate Cyclase ◽  
Testicular Tissue ◽  
Signaling System ◽  
Hormone Sensitivity ◽  
Streptozotocin Induced Diabetes ◽  
Adenylate Cyclase Signaling System

Stimulation of Ca2+ influx in αT3–1 gonadotrophs via the cAMP/PKA signaling system

1997 ◽  
Vol 273 (5) ◽  
pp. E850-E858 ◽  
Author(s):  
Marjan Hezareh ◽  
Werner Schlegel ◽  
Stephen R. Rawlings
Keyword(s):  
Adenylate Cyclase ◽  
Calcium Concentration ◽  
Cytosolic Calcium ◽  
Camp Signaling ◽  
Signaling System ◽  
Cyclic Monophosphate ◽  
Pituitary Adenylate Cyclase ◽  
Inositol 1,4,5 Trisphosphate ◽  
Made In ◽  
Stimulation Of

To investigate the regulation of free cytosolic calcium concentration ([Ca2+]i) by the adenosine 3′,5′-cyclic monophosphate (cAMP) signaling system in clonal gonadotrophs, microfluorimetric recordings were made in single indo 1-loaded αT3–1 cells. Forskolin, 8-bromoadenosine 3′,5′-cyclic monophosphate, or a low concentration (100 pM) of the hypothalamic factor pituitary adenylate cyclase-activating polypeptide (PACAP) stimulated Ca2+ step responses or repetitive Ca2+ transients, which were blocked by the removal of extracellular Ca2+ by the dihydropyridine (DHP) (+)PN 200–110 or by preincubation with the protein kinase A (PKA) antagonist H-89 (10 μM). Thus activation of the cAMP/PKA system in αT3–1 gonadotrophs stimulates Ca2+ influx through DHP-sensitive (L-type) Ca2+ channels. In contrast, high PACAP concentrations (100 nM) stimulated biphasic Ca2+ spike-plateau responses. The Ca2+ spike was independent of extracellular Ca2+, and similar responses were observed by microperfusion of individual cells withd- myo-inositol 1,4,5-trisphosphate, suggesting the involvement of the phospholipase C (PLC) signaling pathway. The Ca2+plateau depended on Ca2+ influx, was blocked by (+)PN 200–110, but was only partially blocked by H-89 pretreatment. In conclusion, PACAP stimulates [Ca2+]iincreases in αT3–1 gonadotrophs through both the PLC and adenylate cyclase signaling pathways. Furthermore, this is the first clear demonstration that the cAMP/PKA system can mediate changes in [Ca2+]iin gonadotroph-like cells.

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