Lesion Models

The functional and structural integrity of the DLPFC is critical for working memory. Alterations in dopamine input to, or turnover within, the DLPFC disrupt normal working memory. In experimental animals, lesions of the dopamine cells innervate the DLPFC, and lesions of the DLPFC increase dopamine turnover and impair working memory in ways similar to pharmacological manipulations of the dopamine system (Funahashi et al., 1993; Murphy et al., 1996). In both rats and monkeys the cognitive deficits induced by increased dopamine turnover in the DLPFC can be prevented by treatment with haloperidol and clozapine. Thus, these researchers concluded that dysfunction of the DLPFC may relate to some of the cognitive deficits present in people with schizophrenia.

Lesions of the developing ventral hippocampus in animals have been found to produce a variety of schizophrenia-like abnormalities that change over the life span of the animal (Lipska and Weinberger, 2000). For instance, excitotoxic lesions of the ventral hippocampus initially produce social deficits, followed by motor deficits reminiscent of dopamine hyperactivity, deficits of latent inhibition and PPI, and problems in working memory. Furthermore, many of these lesion-induced behaviors are normalized by antipsychotic agents. Lesions of the ventral hippocampus also produce many neurochemical and electrophysiological changes that are consistent with schizophrenia pathology.

Other lesion models that have been less extensively characterized at this point include excitotoxic lesions of the prefrontal cortex, neonatal intracerebroventricular infusions of kainic acid, and neonatal depletion of serotonin.

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