types of non-NMDA glutamate receptors in the cortex and hippocampus, thereby leading to an amelioration of the symptoms of schizophrenia. It is of interest that there were some subtle differences in the changes in the glutamate receptor subtypes between haloperidol and clozapine which may account for the greater efficacy of clozapine in the treatment of the negative features of schizophrenia. It now remains to be shown that similar changes occur in the schizophrenic patient following therapeutically effective doses of typical and atypical neuroleptics. Nevertheless such studies do help to extend the dopamine hypothesis to explain the neurochemical basis of the positive and negative symptoms, the selectivity of the atypical neuroleptics in ameliorating the negative symptoms and, partly, the reason why it is necessary to administer neuroleptics for several weeks before optimal therapeutic benefit is obtained by the patient. A summary of the evidence implicating changes in dopamine, glutamate 5-HT and GABA in schizophrenia is shown in Table 11.3.
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