RGD Reference Report - Time-dependent alterations of cholinergic markers after experimental traumatic brain injury. - Rat Genome Database

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Time-dependent alterations of cholinergic markers after experimental traumatic brain injury.

Authors: Donat, CK  Schuhmann, MU  Voigt, C  Nieber, K  Deuther-Conrad, W  Brust, P 
Citation: Donat CK, etal., Brain Res. 2008 Dec 30;1246:167-77. Epub 2008 Sep 30.
RGD ID: 5686682
Pubmed: PMID:18848922   (View Abstract at PubMed)
DOI: DOI:10.1016/j.brainres.2008.09.059   (Journal Full-text)

Traumatic brain injury (TBI) is one of the leading causes of death and disability. Cognitive deficits are believed to be connected with impairments of the cholinergic system. The present study was conducted to evaluate the cholinergic system in a model of focal brain injury with special attention to the time course of posttraumatic events in critical brain regions. Three groups of male Sprague-Dawley rats (post-TBI survival time: 2 h, 24 h and 72 h) were subjected to sham-operation (control) or controlled cortical impact injury. Receptor densities were determined on frozen ipsilateral sagittal brain sections with [(3)H]epibatidine (nicotinic acetylcholine receptors) and [(3)H]QNB (muscarinic acetylcholine receptors). The density of the vesicular acetylcholine transporter (vAChT) was evaluated with (-)[(3)H]vesamicol. Compared to control, vAChT was lowered (up to 50%) at each time point after trauma, with reductions in olfactory tubercle, basal forebrain, motor cortex, putamen, thalamic and hypothalamic areas and the gigantocellular reticular nucleus. Time-dependent reductions of about 20% of nAChR-density in the thalamus, hypothalamus, olfactory tubercle, gigantocellular reticular nucleus and motor cortex were observed post-TBI at 24 and 72 h. The same brain regions showed reductions of mAChR at 24 and 72 h after trauma with additional decreases in the corpus callosum, basal forebrain and anterior olfactory nucleus. In conclusion, cholinergic markers showed significant time-dependent impairments after TBI. Considering the role of the cholinergic system for cognitive processes in the brain, it seems likely that these impairments contribute to clinically relevant cognitive deficits.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
SLC18A3HumanBrain Injuries  ISOSlc18a3 (Rattus norvegicus)protein:decreased expression:brainRGD 
Slc18a3RatBrain Injuries  IEP protein:decreased expression:brainRGD 
Slc18a3MouseBrain Injuries  ISOSlc18a3 (Rattus norvegicus)protein:decreased expression:brainRGD 

Objects Annotated

Genes (Rattus norvegicus)
Slc18a3  (solute carrier family 18 member A3)

Genes (Mus musculus)
Slc18a3  (solute carrier family 18 (vesicular monoamine), member 3)

Genes (Homo sapiens)
SLC18A3  (solute carrier family 18 member A3)


Additional Information