Abstract
An impairment of long-term synaptic plasticity is a peculiar endophenotype of distinct forms of dystonia. We previously demonstrated a complete loss of corticostriatal long-term synaptic depression (LTD) in rodent models of two distinct isolated dystonias, resulting from mutations in the TOR1A (DYT1), and GNAL (DYT25) genes. Broad-spectrum antimuscarinic drugs are used to counteract abnormal striatal acetylcholine-mediated transmission, which plays a crucial role in dystonia pathophysiology. The aberrant excitability of striatal cholinergic cells can also be modulated by group I metabotropic glutamate receptor subtypes.
Sign-in/Register to access full text options 
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.
