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Article: Attenuation of the electrophysiological function of the corpus callosum after fluid percussion injury in the rat

TitleAttenuation of the electrophysiological function of the corpus callosum after fluid percussion injury in the rat
Authors
KeywordsCorpus callosum
Traumatic brain injury
Fluid percussion injury model
White matter injury
Electrophysiology
Issue Date2002
Citation
Journal of Neurotrauma, 2002, v. 19, n. 5, p. 587-599 How to Cite?
AbstractThis study describes a new method used to evaluate axonal physiological dysfunction following fluid percussion induced traumatic brain injury (TBI) that may facilitate the study of the mechanisms and novel therapeutic strategies of posttraumatic diffuse axonal injury (DAI). Stimulated compound action potentials (CAP) were recorded extracellularly in the corpus callosum of superfused brain slices at 3 h, and 1, 3, and 7 days following central fluid percussion injury and demonstrated a temporal pattern of functional deterioration. The maximal CAP amplitude (CAPA) covaried with the intensity of impact 1 day following sham, mild (1.0-1.2 atm), and moderate (1.8-2.0 atm) injury (p < 0.05; 1.11 ± 0.10, 0.82 ± 0.11, and 0.49 ± 0.08 mV, respectively). The CAPA in sham animals were approximately 1.1 mV and did not vary with survival interval (3 h, and 1, 3, and 7 days); however, they were significantly decreased at each time point following moderate injury (p < 0.05; 0.51 ± 0.11, 0.49 ± 0.08, 0.46 ± 0.10, and 0.75 ± 0.13 mV, respectively). The CAPA at 7 days in the injured group were higher than at 3 h, and 1 and 3 days. H&E and amyloid precursor protein (APP) light microscopic analysis confirmed previously reported trauma-induced axonal injury in the corpus callosum seen after fluid percussion injury. Increased APP expression was confirmed using Western blotting showing significant accumulation at 1 day (IOD 913.0 ± 252.7; n = 3; p = 0.05), 3 days (IOD 753.1 ± 159.1; n = 3; p = 0.03), and at 7 days (IOD 1093.8 = 105.0; n = 3; p = 0.001) compared to shams (IOD 217.6 ± 20.4; n = 3). Thus, we report the characterization of white matter axonal dysfunction in the corpus callosum following TBI. This novel method was easily applied, and the results were consistent and reproducible. The electrophysiological changes were sensitive to the early effects of impact intensity, as well as to delayed changes occurring several days following injury. They also indicated a greater degree of attenuation than predicted by APP expression changes alone.
Persistent Identifierhttp://hdl.handle.net/10722/205693
ISSN
2015 Impact Factor: 4.377
2015 SCImago Journal Rankings: 1.945
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBaker, Andrew J.-
dc.contributor.authorPhan, Nicolas-
dc.contributor.authorMoulton, Richard J.-
dc.contributor.authorFehlings, Michael George-
dc.contributor.authorYücel, Yeni H.-
dc.contributor.authorZhao, Min-
dc.contributor.authorLiu, Elaine-
dc.contributor.authorTian, Guofeng-
dc.date.accessioned2014-10-06T08:02:13Z-
dc.date.available2014-10-06T08:02:13Z-
dc.date.issued2002-
dc.identifier.citationJournal of Neurotrauma, 2002, v. 19, n. 5, p. 587-599-
dc.identifier.issn0897-7151-
dc.identifier.urihttp://hdl.handle.net/10722/205693-
dc.description.abstractThis study describes a new method used to evaluate axonal physiological dysfunction following fluid percussion induced traumatic brain injury (TBI) that may facilitate the study of the mechanisms and novel therapeutic strategies of posttraumatic diffuse axonal injury (DAI). Stimulated compound action potentials (CAP) were recorded extracellularly in the corpus callosum of superfused brain slices at 3 h, and 1, 3, and 7 days following central fluid percussion injury and demonstrated a temporal pattern of functional deterioration. The maximal CAP amplitude (CAPA) covaried with the intensity of impact 1 day following sham, mild (1.0-1.2 atm), and moderate (1.8-2.0 atm) injury (p < 0.05; 1.11 ± 0.10, 0.82 ± 0.11, and 0.49 ± 0.08 mV, respectively). The CAPA in sham animals were approximately 1.1 mV and did not vary with survival interval (3 h, and 1, 3, and 7 days); however, they were significantly decreased at each time point following moderate injury (p < 0.05; 0.51 ± 0.11, 0.49 ± 0.08, 0.46 ± 0.10, and 0.75 ± 0.13 mV, respectively). The CAPA at 7 days in the injured group were higher than at 3 h, and 1 and 3 days. H&E and amyloid precursor protein (APP) light microscopic analysis confirmed previously reported trauma-induced axonal injury in the corpus callosum seen after fluid percussion injury. Increased APP expression was confirmed using Western blotting showing significant accumulation at 1 day (IOD 913.0 ± 252.7; n = 3; p = 0.05), 3 days (IOD 753.1 ± 159.1; n = 3; p = 0.03), and at 7 days (IOD 1093.8 = 105.0; n = 3; p = 0.001) compared to shams (IOD 217.6 ± 20.4; n = 3). Thus, we report the characterization of white matter axonal dysfunction in the corpus callosum following TBI. This novel method was easily applied, and the results were consistent and reproducible. The electrophysiological changes were sensitive to the early effects of impact intensity, as well as to delayed changes occurring several days following injury. They also indicated a greater degree of attenuation than predicted by APP expression changes alone.-
dc.languageeng-
dc.relation.ispartofJournal of Neurotrauma-
dc.subjectCorpus callosum-
dc.subjectTraumatic brain injury-
dc.subjectFluid percussion injury model-
dc.subjectWhite matter injury-
dc.subjectElectrophysiology-
dc.titleAttenuation of the electrophysiological function of the corpus callosum after fluid percussion injury in the rat-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1089/089771502753754064-
dc.identifier.pmid12042094-
dc.identifier.scopuseid_2-s2.0-0036267103-
dc.identifier.volume19-
dc.identifier.issue5-
dc.identifier.spage587-
dc.identifier.epage599-
dc.identifier.isiWOS:000175915900004-

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