Abstract
Animal models are critical for the study of psychiatric disorders since they allow the use of invasive methods that cannot be used for ethical reasons in humans. Currently there are three general models of schizophrenia; (i) those produced with acute pharmacological intervention (i.e. MK-801, ketamine, PCP and amphetamine), (ii) genetic models (i.e. mutant DISC-1, D(2)-R over expression) and (iii) developmental disruption models (i.e. MAM, neonatal ventral hippocampal lesion, isolation rearing, maternal infection). Here we review evidence for the validity of gestational (day 17) MAM administration as a developmental disruption rodent model of schizophrenia. Offspring from MAM-treated dams are reported to display deficits consistent with those observed in schizophrenia patients, including anatomical changes, behavioral deficits and altered neuronal information processing. Thus gestational MAM administration has been demonstrated to induce a pathodevelopmental process leading to neuroanatomical and behavioral phenotypes consistent with that observed in schizophrenia in humans.