KAINIC ACID LESIONS IN ADULT RATS AS A MODEL OF SCHIZOPHRENIA - CHANGES IN AUDITORY INFORMATION-PROCESSING

Previous studies have suggested that intracerebroventricular kainic ac id injections alter brain anatomy and neurochemistry in a manner simil ar to what is observed in schizophrenic patients. Disturbances in sens ory information processing are one of the major symptoms of schizophre nia. Thus, the present experiments were designed to evaluate the hypot hesis that hippocampal damage, induced by administration of kainic aci d, would alter the processing of auditory stimuli in a paired-click pa radigm. Adult male Sprague-Dawley rats were implanted for surface reco rding of auditory evoked potentials. At the time of electrode implanta tion, the rats also received bilateral injections of either kainic aci d or the vehicle solution. In vehicle-treated rats, the midlatency N40 component of the auditory evoked potential was diminished in amplitud e by approximately 60% in response to the second of a pair of clicks d elivered 0.5 s apart. By contrast, no reduction of the N40 wave evoked by the second click was observed in kainate-treated rats. Further, ad ministration of haloperidol, a prototypical neuroleptic agent, did not improve this auditory processing dysfunction in kainate-treated anima ls. Loss of auditory filtering in the paired-click paradigm and a lack of response to haloperidol in this test are typically observed in sch izophrenic humans. Thus, the present results demonstrate that kainate- lesioned rats possess a functional schizophrenia-like abnormality, fur ther reinforcing the utility of this model system for studying the bas ic neurobiology of schizophrenia-induced sensory processing deficits. (C) 1997 IBRO. Published by Elsevier Science Ltd.