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PMID:17540347

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Citation

Lee, PR, Brady, DL, Shapiro, RA, Dorsa, DM and Koenig, JI (2007) Prenatal stress generates deficits in rat social behavior: Reversal by oxytocin. Brain Res. 1156:152-67

Abstract

Neurodevelopmental changes induced by environmental stress exposure play a significant but poorly defined role in the etiology of schizophrenia. Exposure of pregnant female rats to a series of unpredictable stresses during the final week of pregnancy generates behavioral deficits and molecular changes in the offspring similar to those observed in schizophrenic individuals. We used this rat prenatal stress preparation to investigate social withdrawal behaviors that may have relevance to the negative symptoms of schizophrenia. The cumulative time adult male offspring of stress-exposed pregnant female rats actively interacted with a weight-matched, same-sex peer was decreased approximately 76% relative to non-stress exposed control rats. Prenatal stress exposure also diminished the quality of the social interaction behavior indicative of reduced social drive. Analysis of the oxytocinergic system in the prenatally stressed male rats revealed significantly less oxytocin mRNA in the paraventricular nucleus and increased oxytocin receptor binding in the central amygdala. Moreover, oxytocin, but not vasopressin, administration into the central amygdala reversed the social incompetence of the prenatally stressed rats without increasing behavior in non-stressed control animals. In addition, cross-fostering pups from prenatally stressed mothers to non-stressed mothers failed to improve the social deficit of the prenatally stressed male offspring. Two behavioral assays designed to measure anxiety did not differentiate the prenatally stressed rats from non-stressed controls. These data indicate that prenatal stress may be an etiologically appropriate animal model for some aspects of schizophrenic social withdrawal. Furthermore, unpredictable prenatal stress exposure selectively degrades social interaction behaviors without increasing anxiety measures.

Links

PubMed PMC2270791 Online version:10.1016/j.brainres.2007.04.042

Keywords

Amygdala/drug effects; Amygdala/embryology; Amygdala/physiology; Animals; Disease Models, Animal; Female; Humans; Hypothalamus/drug effects; Hypothalamus/embryology; Hypothalamus/physiology; Oxytocin/pharmacology; Pregnancy; Pregnancy Complications/psychology; Prenatal Exposure Delayed Effects; Rats; Schizophrenic Psychology; Social Behavior; Stress, Physiological/embryology; Stress, Physiological/prevention & control; Stress, Physiological/psychology

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

RAT:NEU1

involved_in

GO:0035176: social behavior

ECO:0000314: direct assay evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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