title: The MAM rodent model of schizophrenia.
abstract: Rodent models of human disease are essential to obtain a better understanding of disease pathology, the mechanism of action underlying conventional treatments, as well as for the generation of novel therapeutic approaches. There are a number of rodent models of schizophrenia based on either genetic manipulations, acute or sub-chronic drug administration, or developmental disturbances. The prenatal methylazoxymethanol acetate (MAM) rodent model is a developmental disruption model gaining increased attention because it displays a number of histological, neurophysiological, and behavioral deficits analogous to those observed in schizophrenia patients. This unit describes the procedures required to safely induce the MAM phenotype in rats. In addition, we describe a simple behavioral procedure, amphetamine-induced hyperlocomotion, which can be utilized to verify the MAM phenotype.
authors.affiliation: Department of Pharmacology and Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA.
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Lodge
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects; D002985:Clinical Protocols; D004195:Disease Models, Animal; D005260:Female; D047109:Fetal Development / Q000187:drug effects; D008297:Male; D008746:Methylazoxymethanol Acetate; D009498:Neurotoxins; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012559:Schizophrenia / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology
chemical_list: D009498:Neurotoxins; D008746:Methylazoxymethanol Acetate
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