title: The role of stress and dopamine-GABA interactions in the vulnerability for schizophrenia.
abstract: Current hypotheses concerning the etiology of schizophrenia often invoke both an abnormal gene(s) and an environmental disturbance as necessary components to the vulnerability for this disorder. According to one model of schizophrenia presented here, the putative environmental factor may consist of stress and require both pre- and post-natal exposure for a "mis-wiring" of dopaminergic inputs to GABAergic neurons of the cortex to occur. Since the cortical dopamine system continues to mature until the start of the early adult period, the normal ingrowth of dopamine fibers during late adolescence and their formation of aberrant connections with abnormal intrinsic corticolimbic circuits could "trigger" the onset of symptoms in those who carry the constitutional vulnerability for schizophrenia.
authors.affiliation: Laboratory for Structural Neuroscience, McLean Hospital, Belmont, MA 02178, U.S.A.
authors.forename: F M
authors.initials: FM
authors.lastname: Benes
mesh_terms: D000293:Adolescent; D000328:Adult; D001143:Arousal / Q000235:genetics / Q000502:physiology*; D002540:Cerebral Cortex / Q000503:physiopathology; D002648:Child; D002675:Child, Preschool; D004298:Dopamine / Q000502:physiology*; D005260:Female; D015870:Gene Expression / Q000502:physiology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008032:Limbic System / Q000503:physiopathology; D008297:Male; D009415:Nerve Net / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000235:genetics / Q000502:physiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors; D012559:Schizophrenia / Q000235:genetics / Q000503:physiopathology*; D012565:Schizophrenic Psychology; D012931:Social Environment; D013315:Stress, Psychological / Q000150:complications* / Q000503:physiopathology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
chemical_list: D005680:gamma-Aminobutyric Acid; D004298:Dopamine