AbstractScopolamine, a non‐selective muscarinic antagonist at M1and M2receptors, has been shown to cause hyperactivity and memory deficits in rodents. However, the relative role of activation at M1and M2receptors is unclear. The effects in rats of a putative M1antagonist 3‐quinuclidinyl‐xanthene‐9‐carboxylate hemioxalate hydrate (QNX) were assessed in a paradigm that measures locomotion and habituation, a form of non‐associative learning, to a locomotor activity box. On day 1, subcutaneous administration of QNX (1.0 mg/kg) elicited a large (370%) increase in locomotion. On day 2, control animals demonstrated habituation 24 hr after their first exposure to the locomotor box, as shown by significant decreases (−47%) in locomotor activity, while on day 2 the locomotor activity scores of animals that had been treated on the previous day with QNX did not differ from the day 1 scores of control animals. The selective M1agonist 4‐(m‐chlorophenylcarbamoyloxy)‐2‐butynyl‐trimethyl ammonium chloride (McN‐A‐343, 10.0 mg/kg) significantly attenuated both the QNX‐induced locomotion and habituation deficit, while neither the non‐selective muscarinic agonist oxotremorine (0.125 mg/kg) nor the acetylcholinesterase inhibitor physostigmine (0.06 mg/kg) had a significant effect on these behaviors. These data suggest that, in this model, the M1cholinergic receptor mediates both locomotion and habituation. Furthermore, M1agonists can be identified by reversal of both QNX‐induced locomotion and