Journal
NEUROSCIENCE
Volume 144, Issue 1, Pages 38-45Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2006.09.009
Keywords
oxytocin; vasopressin; dopamine; monogamy; pair-bonding; development
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Funding
- NICHD NIH HHS [F32 HD08702, F32 HD008702, P01 HD038490, P01 HD38490] Funding Source: Medline
- NIMH NIH HHS [R01 MH073022, R01 MH056538, MH073022, R01 MH056539, MH 56539] Funding Source: Medline
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Developmental exposure to oxytocin (OT) or oxytocin antagonists (OTAs) has been shown to cause longlasting and often sexually dimorphic effects on social behaviors in prairie voles (Microtus ochrogaster). Because regulation of social behavior in monogamous mammals involves central receptors for OT, arginine vasopressin (AVP), and dopamine, we examined the hypothesis that the long-lasting, developmental effects of exposure to neonatal OT or OTA might reflect changes in the expression of receptors for these peptides. On postnatal day 1, prairie voles were injected intraperitoneally with either OT (1 mg/kg), an OTA (0.1 mg/kg), saline vehicle, or were handled only. At approximately 60 days of age, vasopressin V1a receptors, OT receptors (OTR) and dopamine D2 receptor binding were quantified using receptor autoradiography in brain tissue taken from males and females. Significant treatment effects on V1a binding were found in the bed nucleus of the stria terminalis (BNST), cingulate cortex (CgCtx), mediodorsal thalamus (MdThal), medial preoptic area of the hypothalamus (MPOA), and lateral septum (LS). The CgCtx, MPOA, ventral pallidum, and LS also showed significant sex by treatment interactions on V1a binding. No significant treatment or sex differences were observed for D2 receptor binding. No significant treatment difference was observed for OTR receptor binding, and only a marginal sex difference. Changes in the neuropeptide receptor expression, especially the V1a receptor, may help to explain sexually dimorphic changes in behavior that follow comparable neonatal manipulations. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.
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