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Article: Structural and functional alterations of cerebellum following fluid percussion injury in rats

TitleStructural and functional alterations of cerebellum following fluid percussion injury in rats
Authors
KeywordsPurkinje cell death
Traumatic brain injury
Cerebellum
Climbing fiber
Issue Date2007
Citation
Experimental Brain Research, 2007, v. 177, n. 1, p. 95-112 How to Cite?
AbstractCerebellum was shown to be vulnerable to traumatic brain injury (TBI) in experimental animals. However, the detailed pathological and functional changes within the cerebellum following TBI are not known. Using our established cerebellum fluid percussion injury (FPI) model, we characterized the temporal pattern and the nature of structural damage following FPI, as well as the functional changes of Purkinje cells in response to climbing fiber activation. Our results showed that 60% of Purkinje cells died within the first 24 h following moderate FPI. In contrast, clusters of densely stained shrunken granule cells were stained positive for terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL) in 1, 3 or 7 days following FPI animals. We also observed an accompanying structural damage to the cerebellar white matter tract. Disconnected axonal fibers appeared 1 day post-FPI, and loss of white matter fibers were visible 3 and 7 days post-FPI. Massive accumulation of β-amyloid precursor protein (βAPP) was found in the white matter tracts and molecular layer in the cerebellum of 1, 3 or 7 days FPI animals. Our functional study showed that the majority of Purkinje cells from 1 day and all cells from 3 to 7 days post-FPI had distorted membrane potential and synaptic responses to climbing fiber activation. These results suggested that there is a co-related structural and functional deterioration with a specific temporal pattern in the cerebellum following FPI. These observations provide a basis for future mechanistic investigations aiming to realize neuroprotection from cerebellar neuronal death and loss of cerebellar functionality. © 2006 Springer-Verlag.
Persistent Identifierhttp://hdl.handle.net/10722/205702
ISSN
2015 Impact Factor: 2.057
2015 SCImago Journal Rankings: 1.140
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAi, Jinglu-
dc.contributor.authorLiu, Elaine-
dc.contributor.authorPark, Eugene-
dc.contributor.authorBaker, Andrew J.-
dc.date.accessioned2014-10-06T08:02:13Z-
dc.date.available2014-10-06T08:02:13Z-
dc.date.issued2007-
dc.identifier.citationExperimental Brain Research, 2007, v. 177, n. 1, p. 95-112-
dc.identifier.issn0014-4819-
dc.identifier.urihttp://hdl.handle.net/10722/205702-
dc.description.abstractCerebellum was shown to be vulnerable to traumatic brain injury (TBI) in experimental animals. However, the detailed pathological and functional changes within the cerebellum following TBI are not known. Using our established cerebellum fluid percussion injury (FPI) model, we characterized the temporal pattern and the nature of structural damage following FPI, as well as the functional changes of Purkinje cells in response to climbing fiber activation. Our results showed that 60% of Purkinje cells died within the first 24 h following moderate FPI. In contrast, clusters of densely stained shrunken granule cells were stained positive for terminal deoxynucleotidyl transferase-mediated UTP nick end labeling (TUNEL) in 1, 3 or 7 days following FPI animals. We also observed an accompanying structural damage to the cerebellar white matter tract. Disconnected axonal fibers appeared 1 day post-FPI, and loss of white matter fibers were visible 3 and 7 days post-FPI. Massive accumulation of β-amyloid precursor protein (βAPP) was found in the white matter tracts and molecular layer in the cerebellum of 1, 3 or 7 days FPI animals. Our functional study showed that the majority of Purkinje cells from 1 day and all cells from 3 to 7 days post-FPI had distorted membrane potential and synaptic responses to climbing fiber activation. These results suggested that there is a co-related structural and functional deterioration with a specific temporal pattern in the cerebellum following FPI. These observations provide a basis for future mechanistic investigations aiming to realize neuroprotection from cerebellar neuronal death and loss of cerebellar functionality. © 2006 Springer-Verlag.-
dc.languageeng-
dc.relation.ispartofExperimental Brain Research-
dc.subjectPurkinje cell death-
dc.subjectTraumatic brain injury-
dc.subjectCerebellum-
dc.subjectClimbing fiber-
dc.titleStructural and functional alterations of cerebellum following fluid percussion injury in rats-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00221-006-0654-9-
dc.identifier.pmid16924485-
dc.identifier.scopuseid_2-s2.0-33846694630-
dc.identifier.volume177-
dc.identifier.issue1-
dc.identifier.spage95-
dc.identifier.epage112-
dc.identifier.isiWOS:000243905300008-

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