4.1 Article

Neuropeptides and the social brain: potential rodent models of autism

Journal

INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
Volume 23, Issue 2-3, Pages 235-243

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.ijdevneu.2004.05.006

Keywords

vasopressin VIa receptor; oxytocin receptor; social memory; knockout mice; pair bond; vole; oxytocin; vasopressin; neuropeptides

Funding

  1. NCRR NIH HHS [RR00165] Funding Source: Medline
  2. NIMH NIH HHS [MH56538, MH56897, MH64692, MH65050, MH070112] Funding Source: Medline

Ask authors/readers for more resources

Conducting basic scientific research on a complex psychiatric disorder, such as autism, is a challenging prospect. It is difficult to dissociate the fundamental neurological and psychological processes that are disturbed in autism and, therefore, it is a challenge to discover accurate and reliable animal models of the disease. Because of their role in animal models of social processing and social bonding, the neuropeptides oxytocin and vasopressin are strong candidates for dysregulation in autism. In this review, we discuss the current animal models which have investigated oxytocin and vasopressin systems in the brain and their effects on social behavior. For example, mice lacking the oxytocin gene have profound deficits in social processing and social recognition, as do rats lacking vasopressin or mice lacking the vasopressin V I a receptor (V1aR). In another rodent model, monogamous prairie voles are highly social and form strong pair bonds with their mates. Pair bonds can be facilitated or disrupted by perturbing the oxytocin and vasopressin systems. Non-monogamous vole species that do not pair bond have different oxytocin and V1aR distribution patterns in the brain than monogamous vole species. Potential ties from these rodent models to the human autistic condition are then discussed. Given the hallmark disturbances in social function, the study of animal models of social behavior may provide novel therapeutic targets for the treatment of autism. (C) 2004 ISDN. Published by Elsevier Ltd. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.1
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available