Adenylate cyclase and G-proteins as a signal transfer system in the guinea pig inner ear

1988 ◽  
Vol 245 (2) ◽  
pp. 82-87 ◽  
Author(s):  
T. Koch ◽  
H. -P. Zenner
1979 ◽  
Vol 222 (4) ◽  
pp. 275-283 ◽  
Author(s):  
Hans -Peter Zenner ◽  
Birgit Zenner

1987 ◽  
Vol 103 (5) ◽  
pp. 204-211 ◽  
Author(s):  
B. Erlandsson ◽  
H. Hakanson ◽  
A. Ivarsson ◽  
P. Nilsson ◽  
J. Wersall

1982 ◽  
Vol 234 (2) ◽  
pp. 125-130 ◽  
Author(s):  
Matti Anniko ◽  
Aron Sobin ◽  
Romuald Wr�blewski
Keyword(s):  
X Ray ◽  

1991 ◽  
Vol 276 (3) ◽  
pp. 683-689 ◽  
Author(s):  
J G Kiang ◽  
Y Y Wu ◽  
M C Lin

The basal level of intracellular cyclic AMP (cAMPi) in A-431 cells incubated at 37 degrees C in Na(+)-containing Hanks solution is 2086 +/- 139 fmol/10(6) cells. When cells are exposed to 45 degrees C for 10 min, cAMPi increases by 40 +/- 4%, and then returns to basal levels within 30 min. Incubating cells in Ca(2+)-free or Mg(2+)-free Hanks solution has no effect on the heat-induced increase in cAMPi, but the increase is inhibited by acid-loading cells to intracellular pH 7.0 or 6.8. In unheated cells, cAMPi increases by 16 +/- 8%, 53 +/- 7%, or 39 +/- 8%, when incubated with isobutyl-1-methylxanthine (1 mM), Ro 20-1724 (0.5 mM), or theophylline (1 mM) respectively. However, heat treatment further elevates cAMPi in cells treated with phosphodiesterase inhibitors, indicating that heat treatment and phosphodiesterase inhibitors elevate cAMPi by a different pathway(s). Heat treatment increases adenylate cyclase activity 2.5-fold. When forskolin (150 microM), an adenylate cyclase stimulator, is applied to cells, the basal cAMPi increases 28 +/- 6-fold compared with controls. Subsequent heating of these cells lowers cAMPi levels to 7.0 +/- 0.5 times that in control cells. This decrease is prevented by pretreatment with pertussis toxin (30 ng/ml, 24 h), suggesting that G-proteins are involved in the process of heat-induced cAMPi increase. 2-Deoxy-D-glucose (10 mM), NaN3 (10 mM) and 2,4-dinitrophenol (1 mM) also increase cAMPi in A-431 cells. However, application of these metabolic inhibitors to cells before heat treatment does not result in cAMPi levels greater than that observed in cells with heat alone. Similar observations are obtained in heat-treated cells previously exposed to adenosine, but not to AMP or ADP. These data are the first to suggest that thermally induced increase in cAMPi is due to a combination of activation of adenylate cyclase and G-proteins, and an increase in adenosine owing to ATP breakdown caused by hyperthermia.


2006 ◽  
Vol 281 (40) ◽  
pp. 30234-30241 ◽  
Author(s):  
Rolf Herrmann ◽  
Martin Heck ◽  
Peter Henklein ◽  
Klaus Peter Hofmann ◽  
Oliver P. Ernst
Keyword(s):  

1982 ◽  
Vol 60 (3) ◽  
pp. 302-307 ◽  
Author(s):  
M. J. York ◽  
L. P. Davies

We have used the adenosine-stimulated adenylate cyclase of guinea-pig brain to examine the potency of diazepam as an adenosine uptake inhibitor. Diazepam at concentrations in the range 10–500 μM stimulates the production of cAMP in incubated slices of guinea-pig cerebral cortex, with maximal fivefold stimulations over basal levels by 200 μM diazepam. The increases can be largely (but not completely) blocked by the adenosine antagonist theophylline or by addition of excess adenosine deaminase to the system. It appears that the stimulation of cAMP production is due to a blockade of adenosine uptake which results in an increase in extracellular adenosine and concomitant activation of the adenosine receptor coupled to adenylate cyclase. Since the cAMP response to standard adenosine uptake blockers (dipyridamole, dilazep) can be completely blocked by theophylline or adenosine deaminase, a small component of the diazepam response cannot be explained by an adenosine effect. The concentration of diazepam at which the first significant cAMP increase occurs is 10 μM or slightly lower. This is significantly higher than the concentration of diazepam needed to saturate the pharmacologically characterized central nervous system receptors for benzodiazepines.


2010 ◽  
Vol 130 (8) ◽  
pp. 868-880
Author(s):  
Lishu Li ◽  
Tetsuo Ikezono ◽  
Kuwon Sekine ◽  
Susumu Shindo ◽  
Tomohiro Matsumura ◽  
...  

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