"Selective inhibition of striatal fast-spiking interneurons elicits dystonia"
dc.contributor.author | Gittis, AH | |
dc.contributor.author | Leventhal, DK | |
dc.contributor.author | Fensterheim, BA | |
dc.contributor.author | Pettibone, JR | |
dc.contributor.author | Berke, JD | |
dc.contributor.author | Kreitzer, AC | |
dc.coverage.spatial | Washington, D.C. | |
dc.date.accessioned | 2023-08-01T13:22:00Z | |
dc.date.available | 2023-08-01T13:22:00Z | |
dc.date.issued | 2011-11-02 | |
dc.identifier.issn | 0270-6474 | |
dc.identifier.issn | 1529-2401 | |
dc.identifier.uri | https://www.ncbi.nlm.nih.gov/pubmed/22049415 | |
dc.identifier.uri | https://hdl.handle.net/2027.42/177391 | en |
dc.description.abstract | Fast-spiking interneurons (FSIs) can exert powerful control over striatal output, and deficits in this cell population have been observed inhuman patients with Tourette syndrome and rodent models of dystonia. However, a direct experimental test of striatal FSI involvementin motor control has never been performed. We applied a novel pharmacological approach to examine the behavioral consequences ofselective FSI suppression in mouse striatum. IEM-1460, an inhibitor of GluA2-lacking AMPARs, selectively blocked synaptic excitation ofFSIs but not striatal projection neurons. Infusion of IEM-1460 into the sensorimotor striatum reduced the firing rate of FSIs but not othercell populations, and elicited robust dystonia-like impairments. These results provide direct evidence that hypofunction of striatal FSIscan produce movement abnormalities, and suggest that they may represent a novel therapeutic target for the treatment of hyperkineticmovement disorders. © 2011 the authors. | |
dc.format.medium | ||
dc.publisher | Society for Neuroscience | |
dc.rights | Licence for published version: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International | |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | |
dc.subject | Action Potentials | |
dc.subject | Adamantane | |
dc.subject | Analysis of Variance | |
dc.subject | Animals | |
dc.subject | Area Under Curve | |
dc.subject | Cholinergic Antagonists | |
dc.subject | Corpus Striatum | |
dc.subject | Disease Models, Animal | |
dc.subject | Dose-Response Relationship, Drug | |
dc.subject | Drug Interactions | |
dc.subject | Dyskinesias | |
dc.subject | Excitatory Amino Acid Antagonists | |
dc.subject | Excitatory Postsynaptic Potentials | |
dc.subject | Female | |
dc.subject | Functional Laterality | |
dc.subject | Green Fluorescent Proteins | |
dc.subject | Interneurons | |
dc.subject | LIM-Homeodomain Proteins | |
dc.subject | Male | |
dc.subject | Mecamylamine | |
dc.subject | Mice | |
dc.subject | Mice, Transgenic | |
dc.subject | N-Methylaspartate | |
dc.subject | Nerve Tissue Proteins | |
dc.subject | Scopolamine | |
dc.subject | Transcription Factors | |
dc.title | "Selective inhibition of striatal fast-spiking interneurons elicits dystonia" | |
dc.type | Conference Paper | |
dc.identifier.pmid | 22049415 | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/177391/2/15727.full.pdf | |
dc.identifier.doi | 10.1523/JNEUROSCI.3875-11.2011 | |
dc.identifier.doi | https://dx.doi.org/10.7302/7988 | |
dc.identifier.source | Journal of Neuroscience | |
dc.description.version | Published version | |
dc.date.updated | 2023-08-01T13:21:58Z | |
dc.identifier.orcid | 0000-0001-8174-5933 | |
dc.description.filedescription | Description of 15727.full.pdf : Published version | |
dc.identifier.volume | 31 | |
dc.identifier.issue | 44 | |
dc.identifier.startpage | 15727 | |
dc.identifier.endpage | 15731 | |
dc.identifier.name-orcid | Gittis, AH | |
dc.identifier.name-orcid | Leventhal, DK; 0000-0001-8174-5933 | |
dc.identifier.name-orcid | Fensterheim, BA | |
dc.identifier.name-orcid | Pettibone, JR | |
dc.identifier.name-orcid | Berke, JD | |
dc.identifier.name-orcid | Kreitzer, AC | |
dc.working.doi | 10.7302/7988 | en |
dc.owningcollname | Neurology, Department of |
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