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Forskolin markedly stimulates striatal adenylate cyclase activity in a concentration-dependent manner, and at 10(-4) M produces an approximate 40-fold increase in enzyme activity above basal levels. Dopamine (in the presence of 100 nM SCH 23390), bromocryptine and quinpirole (LY 171555) significantly inhibit both basal and forskolin-stimulated adenylate cyclase activity. There is a significant increase in the absolute but not in the percent inhibition of enzyme activity by dopaminergic agonists as a function of forskolin concentration. This inhibition is agonist-concentration dependent and antagonized by the D2 antagonist, spiperone. These results suggest that forskolin may be used as a tool for amplifying the abolute D2-receptor-mediated inhibition of adenylate cyclase in rat striatal homogenates.
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
February 1988,
European journal of pharmacology,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
May 1997,
Journal of neuroscience research,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
May 1989,
Journal of neurochemistry,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
December 1985,
European journal of pharmacology,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
November 1989,
Chemical & pharmaceutical bulletin,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
January 1984,
Neuropsychobiology,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
September 1996,
British journal of pharmacology,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
March 1992,
Zhongguo yao li xue bao = Acta pharmacologica Sinica,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
December 1987,
Neuroscience letters,
G Battaglia, and
A B Norman, and
E J Hess, and
I Creese
July 1986,
The Journal of pharmacology and experimental therapeutics,
