Nimodipine ameliorates impaired eyeblink classical conditioning in older rabbits in the long-delay paradigm

Research using the hippocampally dependent short-conditioned stimulus trace conditioning paradigm demonstrated that nimodipine ameliorated learning deficits in older rabbits. Evidence from in vitro and in vivo measures indicated that the site of drug action was hippocampal pyramidal cells. Acquisition occurs in the long (750 ms) delay conditioning paradigm in the absence of the hippocampus. This experiment with 40 older rabbits was undertaken to determine if nimodipine ameliorates impaired acquisition in a conditioning paradigm not dependent on the hippocampus. Fifteen 90-trial sessions of paired conditioning stimuli were presented to 3 groups receiving daily injections of 0, 1, or 5 mg/kg nimodipine. Explicitly unpaired control groups received 0 or 5 mg/kg nimodipine. Acquisition with the 5 mg/kg dose was significantly faster. Existing evidence suggested that nimodipine acted in the hippocampus, but we could not rule out the possibility that the drug also affected conditioning via the cerebellum.