Walker BR, Klueger K (2006) Rodent models: Autism and fragile x syndrome. Neuroscience 2006 Abstracts 764.6. Society for Neuroscience, Atlanta, GA.
Summary: While the exact etiology of autism is not known, autism spectrum disorders (ASD) are most commonly characterized by behavioral deficits in social interaction and communication, obsessional mannerisms, behavioral inflexibility, impairments in planning, attention, hyperactivity and a lack of environmental awareness. These behavioral characteristics have been theorized to be the result of altered forebrain and/or cerebellar circuitry and neurotransmitter transmission. There is some evidence to suggest that treatments effective against seizure and mood disorders that alter these specific neuronal populations are also effective against some core behavioral characteristics of persons with ASD. Therefore, in the present study we tested the hypothesis that electrical stimulation of the rat vagus nerve, as it enters the nucleus tractus solitarius (NTS), will ameliorate social behavior deficits caused by forebrain ACh lesions. To this end, we measured social interaction behavior in rats following bilateral i.c.v. injection of 192-IgG saporin (192-sap; 2 µg/side) or saline, and again following electrical stimulation of the vagus nerve/NTS (100-900 microA). As shown by us previously, bilateral 192-sap injections created a significant decrease in social behavior, as compared to controls. Electrical stimulation of the vagus/NTS, however, reduced these social deficits in 192-sap rats, while having no effect on the social interaction of sham controls. These findings suggest that the circuitry mediating the behavioral deficits seen in autism and ASD may functionally overlap with circuitry of seizure and mood disorders. In addition, our results suggest that vagal nerve stimulation (VNS) may be effective in reducing some of these core behavioral features seen in autism and ASD.
Related Products: 192-IgG-SAP (Cat. #IT-01)