vasopressin, oxytocin, and autism

[mwbeah]

neuropeptides and the social brain:

potential rodent models of autism

by

lim mm, bielsky if, young lj.

center for behavioral neuroscience

and

department of psychiatry and behavioral sciences,

emory university, atlanta, ga 30322, usa.

int j dev neurosci. 2005 apr-may;23(2-3):235-43

abstract

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 v1a 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.

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some interesting information, fyi

mike