Atropine slows olfactory bulb kindling while diminished cholinergic innervation does not.

The development of kindled seizures elicited through electrical stimulation of the rat olfactory bulb (OB) was examined under two conditions which decrease cholinergic neurotransmission. Atropine sulfate (25 mg/kg, IP) administered 1 hr prior to stimulation of the OB was found to significantly delay the acquisition of the fully kindled state. In a second experiment, diminished cholinergic innervation of the OB was established using chemical lesions of the basal forebrain cholinergic system. Despite the depletion of acetylcholine (Ach), as determined by acetylcholinesterase (AchE) and choline acetyltransferase (ChAt) assays, no significant alterations in kindling parameters were observed. Based upon these findings we suggest that Ach is not critical to the establishment of an OB kindled focus but is important for the propagation and generalization of epileptiform activity initiated through OB stimulation.