The effect of aging on muscarinic cholinergic receptor function in dissociated cell aggregates of the mouse brain was investigated using two biochemical models, i.e., carbachol-induced accumulation of inositol monophosphates and carbachol-induced desensitization of muscarinic cholinergic receptors as measured by the sequestration of specific 3H-N-methyl-scopolamine binding. While aging strongly reduced carbachol-induced inositol monophosphate accumulation, desensitization was not affected in the brains of aged animals. Chronic treatment of aged mice with the nootropic drug piracetam (500 mg/kg daily PO) significantly elevated the agonist-induced accumulation of inositol monophosphates possibly by increasing the available number of muscarinic cholinergic receptors not being in a desensitized state. The results support the hypothesis that nootropics like piracetam might act in part by restoring age-related deficits of central muscarinic cholinergic receptor function.