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dc.contributor.authorTenney, Jeffrey R.
dc.contributor.authorDuong, Timothy Q.
dc.contributor.authorKing, Jean A.
dc.contributor.authorLudwig, Reinhold
dc.contributor.authorFerris, Craig F.
dc.date2022-08-11T08:08:49.000
dc.date.accessioned2022-08-23T16:09:24Z
dc.date.available2022-08-23T16:09:24Z
dc.date.issued2003-08-16
dc.date.submitted2009-01-13
dc.identifier.citation<p>Epilepsia. 2003 Sep;44(9):1133-40.</p>
dc.identifier.issn0013-9580 (Print)
dc.identifier.doi10.1046/j.1528-1157.2003.61002.x
dc.identifier.pmid12919383
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32683
dc.description.abstractPURPOSE: Functional magnetic resonance imaging (fMRI) was used to identify areas of brain activation during absence seizures in an awake animal model. METHODS: Blood-oxygenation-level-dependent (BOLD) fMRI in the brain was measured by using T2*-weighted echo planar imaging at 4.7 Tesla. BOLD imaging was performed before, during, and after absence seizure induction by using gamma-butyrolactone (GBL; 200 mg/kg, intraperitoneal). RESULTS: The corticothalamic circuitry, critical for spike-wave discharge (SWD) formation in absence seizure, showed robust BOLD signal changes after GBL administration, consistent with EEG recordings in the same animals. Predominantly positive BOLD changes occurred in the thalamus. Sensory and parietal cortices showed mixed positive and negative BOLD changes, whereas temporal and motor cortices showed only negative BOLD changes. CONCLUSIONS: With the BOLD fMRI technique, we demonstrated signal changes in brain areas that have been shown, with electrophysiology experiments, to be important for generating and maintaining the SWDs that characterize absence seizures. These results corroborate previous findings from lesion and electrophysiological experiments and show the technical feasibility of noninvasively imaging absence seizures in fully conscious rodents.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12919383&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1046/j.1528-1157.2003.61002.x
dc.subjectAnesthesia; Animals; Cerebral Cortex; Electroencephalography; Epilepsy, Absence; Magnetic Resonance Imaging; Male; Neural Pathways; Rats; Rats, Sprague-Dawley; Thalamus; Wakefulness
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleCorticothalamic modulation during absence seizures in rats: a functional MRI assessment
dc.typeJournal Article
dc.source.journaltitleEpilepsia
dc.source.volume44
dc.source.issue9
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1241
dc.identifier.contextkey693151
html.description.abstract<p>PURPOSE: Functional magnetic resonance imaging (fMRI) was used to identify areas of brain activation during absence seizures in an awake animal model.</p> <p>METHODS: Blood-oxygenation-level-dependent (BOLD) fMRI in the brain was measured by using T2*-weighted echo planar imaging at 4.7 Tesla. BOLD imaging was performed before, during, and after absence seizure induction by using gamma-butyrolactone (GBL; 200 mg/kg, intraperitoneal).</p> <p>RESULTS: The corticothalamic circuitry, critical for spike-wave discharge (SWD) formation in absence seizure, showed robust BOLD signal changes after GBL administration, consistent with EEG recordings in the same animals. Predominantly positive BOLD changes occurred in the thalamus. Sensory and parietal cortices showed mixed positive and negative BOLD changes, whereas temporal and motor cortices showed only negative BOLD changes.</p> <p>CONCLUSIONS: With the BOLD fMRI technique, we demonstrated signal changes in brain areas that have been shown, with electrophysiology experiments, to be important for generating and maintaining the SWDs that characterize absence seizures. These results corroborate previous findings from lesion and electrophysiological experiments and show the technical feasibility of noninvasively imaging absence seizures in fully conscious rodents.</p>
dc.identifier.submissionpathgsbs_sp/1241
dc.contributor.departmentDepartment of Psychiatry
dc.contributor.departmentCenter for Comparative Neuroimaging
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages1133-40


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