scholarly journals Ca2+ stimulation of adenylyl cyclase generates dynamic oscillations in cyclic AMP

2006 ◽  
Vol 119 (5) ◽  
pp. 828-836 ◽  
Author(s):  
D. Willoughby
Keyword(s):  
Cyclic Amp ◽  
Adenylyl Cyclase ◽  
Stimulation Of

Type I adenylyl cyclase functions as a coincidence detector for control of cyclic AMP response element-mediated transcription: synergistic regulation of transcription by Ca2+ and isoproterenol

1994 ◽  
Vol 14 (12) ◽  
pp. 8272-8281
Author(s):  
S Impey ◽  
G Wayman ◽  
Z Wu ◽  
D R Storm
Keyword(s):  
Cyclic Amp ◽  
Adenylyl Cyclase ◽  
Long Term Potentiation ◽  
Regulation Of Transcription ◽  
Type I ◽  
Hek 293 ◽  
293 Cells ◽  
Term Potentiation ◽  
Stimulation Of

Studies carried out with mammals and invertebrates suggest that Ca(2+)-sensitive adenylyl cyclases may be important for neuroplasticity. Long-term potentiation in the hippocampus requires increases in intracellular Ca2+ which are accompanied by elevated cyclic AMP (cAMP). Furthermore, activation of cAMP-dependent protein kinase is required for the late stage of long-term potentiation in the CA1 region of the hippocampus, which is also sensitive to inhibitors of transcription. Therefore, some forms of synaptic plasticity may require coordinate regulation of transcription by Ca2+ and cAMP. In this study, we demonstrate that the expression of type I adenylyl cyclase in HEK-293 cells allows Ca2+ to stimulate reporter gene activity mediated through the cAMP response element. Furthermore, simultaneous activation by Ca2+ and isoproterenol caused synergistic stimulation of transcription in HEK-293 cells and cultured neurons. We propose that Ca2+ and neurotransmitter stimulation of type I adenylyl cyclase may play a role in synaptic plasticity by generating optimal cAMP signals for regulation of transcription.

Prostaglandin Deficiency Promotes Sensitization of Adenylyl Cyclase

2000 ◽  
Vol 381 (5-6) ◽  
pp. 525-529 ◽  
Author(s):  
S. Weber ◽  
H. Lemoine ◽  
H.K. Wasner
Keyword(s):  
Cyclic Amp ◽  
Adenylyl Cyclase ◽  
Adrenergic Receptors ◽  
Type Ii Diabetes ◽  
Plasma Membranes ◽  
Male Rats ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Cyclic Phosphate ◽  
Stimulation Of ◽  
Cyclic Amp Synthesis

Abstract Inhibition of prostaglandin synthesis by the drug indomethacin suppresses the synthesis of the cyclic AMP antagonist, prostaglandylinositol cyclic phosphate (cyclic PIP), and leads to a metabolic state comparable to type II diabetes. It was of interest whether prostaglandindeficiency likewise causes sensitization of adenylyl cyclase, as this has been reported for the diabetic state. In liver plasma membranes of indomethacintreated male rats, basal and forskolinstimulated cyclic AMP synthesis remained unchanged when compared to untreated control rats. In control rats, stimulation of cyclic AMP synthesis by fluoride (2.2-fold) or glucagon (3.5-fold) was much lower than stimulation by forskolin (6.6-fold). In contrast, in indomethacin treated rats, stimulation of cAMP synthesis by fluoride (4.6-fold) or glucagon (5.2-fold) nearly matched the stimulation by forskolin (6.4-fold). The level of α[1]adrenergic receptors was slightly reduced, from 450 to 320 fmol/mg protein, by the indomethacin treatment. Independent of the treatment by indomethacin, stimulation of cyclic AMP synthesis by adrenaline failed, in agreement with the low density of adrenergic βreceptors. In conclusion, PGE deficiency sensitizes adenylyl cyclase in rat liver for G proteincoupled receptors (glucagon) and also for fluoride.

scholarly journals Type I adenylyl cyclase functions as a coincidence detector for control of cyclic AMP response element-mediated transcription: synergistic regulation of transcription by Ca2+ and isoproterenol.

1994 ◽  
Vol 14 (12) ◽  
pp. 8272-8281 ◽  
Author(s):  
S Impey ◽  
G Wayman ◽  
Z Wu ◽  
D R Storm
Keyword(s):  
Cyclic Amp ◽  
Adenylyl Cyclase ◽  
Long Term Potentiation ◽  
Regulation Of Transcription ◽  
Type I ◽  
Hek 293 ◽  
293 Cells ◽  
Term Potentiation ◽  
Stimulation Of

Studies carried out with mammals and invertebrates suggest that Ca(2+)-sensitive adenylyl cyclases may be important for neuroplasticity. Long-term potentiation in the hippocampus requires increases in intracellular Ca2+ which are accompanied by elevated cyclic AMP (cAMP). Furthermore, activation of cAMP-dependent protein kinase is required for the late stage of long-term potentiation in the CA1 region of the hippocampus, which is also sensitive to inhibitors of transcription. Therefore, some forms of synaptic plasticity may require coordinate regulation of transcription by Ca2+ and cAMP. In this study, we demonstrate that the expression of type I adenylyl cyclase in HEK-293 cells allows Ca2+ to stimulate reporter gene activity mediated through the cAMP response element. Furthermore, simultaneous activation by Ca2+ and isoproterenol caused synergistic stimulation of transcription in HEK-293 cells and cultured neurons. We propose that Ca2+ and neurotransmitter stimulation of type I adenylyl cyclase may play a role in synaptic plasticity by generating optimal cAMP signals for regulation of transcription.

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