Abstract
Blockade of ionotropic glutamate receptors can induce changes in central dopamine and glutamate circuits, which model the symptoms of schizophrenia. Nicotine evokes dopamine release through activation of nicotinic acetylcholine receptors, and human research indicates that nicotine improves negative and cognitive symptoms of schizophrenia. The objective was to determine the effect of the glutamate receptor antagonist ketamine on the function of nicotinic receptors that mediate dopamine release. Ketamine (0.1–100 μM) did not evoke [3H]overflow from rat striatal and prefrontal cortical slices preloaded with [3H]dopamine. Subanesthetic ketamine concentrations (1–10 μM) increased nicotine-evoked [3H]overflow. To model the progression of schizophrenia, rats received ketamine (30 mg/kg) or vehicle for 30 days and then nicotine-evoked [3H]overflow was measured. The effect of nicotine was greater in ketamine-treated rats, suggesting that subchronic exposure changes nicotinic receptor activity. Overall, these data indicate that nicotinic receptor function is altered in this model of schizophrenia, and support a role for nicotinic receptors in schizophrenia treatment. MU Psychol Sci Grad Res Grant
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