Prenatal stress generates deficits in rat social behavior: Reversal by oxytocin

Paul R. Lee, Dana L. Brady, Robert A. Shapiro, Daniel Dorsa, James I. Koenig

Research output: Contribution to journalArticle

185 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)152-167
Number of pages16
JournalBrain Research
Volume1156
Issue number1
DOIs
StatePublished - Jul 2 2007

Fingerprint

Social Behavior
Oxytocin
Interpersonal Relations
Schizophrenia
Anxiety
Mothers
Oxytocin Receptors
Foster Home Care
Paraventricular Hypothalamic Nucleus
Environmental Exposure
Adult Children
Systems Analysis
Vasopressins
Animal Models
Weights and Measures
Pregnancy
Messenger RNA

Keywords

  • Amygdala
  • Hypothalamus
  • Oxytocin
  • Prenatal stress
  • Rat
  • Schizophrenia
  • Social interaction

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Developmental Biology
  • Molecular Biology

Cite this

Prenatal stress generates deficits in rat social behavior : Reversal by oxytocin. / Lee, Paul R.; Brady, Dana L.; Shapiro, Robert A.; Dorsa, Daniel; Koenig, James I.

In: Brain Research, Vol. 1156, No. 1, 02.07.2007, p. 152-167.

Research output: Contribution to journalArticle

Lee, Paul R. ; Brady, Dana L. ; Shapiro, Robert A. ; Dorsa, Daniel ; Koenig, James I. / Prenatal stress generates deficits in rat social behavior : Reversal by oxytocin. In: Brain Research. 2007 ; Vol. 1156, No. 1. pp. 152-167.
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