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Properties of Muscarinic‐Stimulated Adenylate Cyclase Activity in Rat Olfactory Bulb
Author(s) -
Olianas Maria C.,
Onali Pierluigi
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb10046.x
Subject(s) - muscarinic acetylcholine receptor , cyclase , olfactory bulb , pertussis toxin , oxotremorine , stimulation , gtp' , medicine , endocrinology , adenylate kinase , chemistry , carbachol , cholera toxin , adenylate cyclase toxin , g protein , biology , biochemistry , receptor , enzyme , central nervous system
The muscarinic stimulation of adenylate cyclase activity in rat olfactory bulb was characterized, with the aim of elucidating the nature of the molecular mechanism involved. Carbachol (CCh) stimulated the enzyme activity in either crude or purified cell membrane preparations and increased cyclic AMP accumulation in miniprisms of olfactory bulb. The CCh stimulation of adenylate cyclase activity displayed a fast onset and was rapidly reversed by addition of atropine. The stimulation was associated with an increase in the apparent V max of the enzyme, with no change in the K m for Mg‐ATP. The affinity of the enzyme for Mg 2+ was enhanced by CCh. The muscarinic effect required GTP at concentrations higher than those needed for enzyme stimulation with either l ‐isoproterenol or vasoactive intestinal peptide. Moreover, contrary to the β‐adrenergic stimulation, the muscarinic effect disappeared when guanosine 5′‐ O ‐(3′‐thiotriphosphate) was substituted for GTP. In vivo treatment of olfactory bulbs with pertussis toxin completely prevented the muscarinic stimulation of adenylate cyclase, whereas cholera toxin was without effect. These results indicate that in rat olfactory bulb muscarinic receptors increase adenylate cyclase activity by interacting with a pertussis toxin‐sensitive GTP‐binding protein different from the stimulatory GTP‐binding protein.