Abstract
The mouse mutant dystonia musculorum shows many of the symptoms of of human dystonics. In this study whole tissue samples of mutant striatum and substantia nigra showed almost 50% less γ-amino butyric acid (GABA) biosynthetic capacity than controls of the same inbred strain. Hypothalamic values were unchanged. The defect appears to be one of substrate localization, since both crude extract enzyme activity and the fractional conversion of glutamate to GABA were unaffected by the mutation. When tissue is disrupted, high-affinity synaptosomal uptake to glutamate does not appear to be affected; therefore an endogenous inhibitor of glutamate transport is postulated for the mutant.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
