Modeling Tourette syndrome pathophysiology through targeted manipulation of striatal interneurons

Pittenger CJ (2015) Modeling Tourette syndrome pathophysiology through targeted manipulation of striatal interneurons. Neuroscience 2015 Abstracts 6.07. Society for Neuroscience, Chicago IL.

Summary: Postmortem studies of Tourette syndrome patients has revealed a reduction in the number of specific striatal interneurons. The authors explored the hypothesis that this neuronal deficit is enough to produce the symptoms of Tourette syndrome in mice. Animals received 90-ng injections of Anti-ChAT-SAP (Cat. #IT-42) into the striatum. Rabbit IgG-SAP (Cat. #IT-35) was used as a control. The data suggest that loss of the striatal interneurons is enough to produce some, but not all, of the symptoms caused by Tourette syndrome.

Related Products: Anti-ChAT-SAP (Cat. #IT-42), Rabbit IgG-SAP (Cat. #IT-35)

See Also:

• Xu M et al. Targeted ablation of cholinergic interneurons in the dorsolateral striatum produces behavioral manifestations of Tourette syndrome. Proc Natl Acad Sci U S A 112:893-898, 2015.