Abstract
Systemic injection of d-amphetamine (1.0 mg/kg) resulted in a progressive increase in locomotor activity as a function of repeated daily drug administration. The magnitude of the stimulant-induced sensitization effect was enhanced by low-current electrical stimulation of the central nucleus of the amygdala during open-field testing. Amygdaloid stimulation in the absence of amphetamine treatment did not influence spontaneous locomotor activity, and there was no behavioral evidence of epileptogenesis following amygdaloid stimulation over the course of the experiment. However, with continued stimulation of the amygdala, early-stage convulsive activity was apparent in animals after approximately 40 days of testing, signifying the advancement of kindling evolution. These results suggest that the processes responsible for kindling acquisition, prior to the behavioral expression of epileptiform events, interact with the underlying substrates of amphetamine sensitization.
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