Prenatal nutritional deprivation as a risk factor in schizophrenia: preclinical evidence.
We will review evidence from preclinical literature that prenatal nutritional deprivation produces neurochemical, morphological, and electrophysiological effects reminiscent of those seen in clinical studies of schizophrenia. We will focus on effects of nutritional deficiency that are likely to have implications for schizophrenia. These include disruption of neurotransmitter systems such as dopamine and serotonin and dysgenesis of the hippocampal formation. Preclinical studies show enhanced release and turnover of dopamine and serotonin following prenatal and early postnatal nutritional deficiency. Morphology of the hippocampus, as well as electrophysiology and hippocampally-mediated behaviors are also altered. Although intriguing, these studies have not been conducted with schizophrenia in mind, and thus, outcome measures that may be more specifically related to schizophrenia have not been examined. We propose that further preclinical studies that examine the consequences of prenatal nutritional deficiency, which may lead to altered neuronal migration and other developmental abnormalities, may be useful in understanding the etiology of schizophrenia.
College of Physicians and Surgeons of Columbia University, New York State Psychiatric Institute, New York.
P D
PD
Butler
E S
ES
Susser
A S
AS
Brown
C A
CA
Kaufmann
J M
JM
Gorman
D000818:Animals; D004298:Dopamine / Q000378:metabolism; D004594:Electrophysiology; D005260:Female; D006624:Hippocampus / Q000196:embryology* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D010927:Placental Insufficiency / Q000150:complications* / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D012559:Schizophrenia / Q000209:etiology* / Q000503:physiopathology; D012701:Serotonin / Q000378:metabolism
D012701:Serotonin; D004298:Dopamine