RGD Reference Report - Time-dependent changes in rat brain cholinergic receptor expression after experimental brain injury. - Rat Genome Database

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Time-dependent changes in rat brain cholinergic receptor expression after experimental brain injury.

Authors: Verbois, SL  Scheff, SW  Pauly, JR 
Citation: Verbois SL, etal., J Neurotrauma. 2002 Dec;19(12):1569-85.
RGD ID: 1599610
Pubmed: PMID:12542858   (View Abstract at PubMed)
DOI: DOI:10.1089/089771502762300238   (Journal Full-text)

Alterations in neurotransmitter receptor expression in the central nervous system may contribute to physiological and behavioral deficits that follow traumatic brain injury (TBI). Previous studies from our laboratory have demonstrated significant and widespread deficits in alpha7* nicotinic cholinergic receptor (alpha7* nAChr) expression 2 days following cortical contusion brain injury. The purpose of this study was to evaluate changes in alpha7* nAChr expression over a wider range of post-TBI recovery intervals. Animals were anesthetized and subjected to a moderate cortical contusion brain injury (2 mm cortical compression). Animals were euthanatized at various post-TBI time intervals, ranging from 1 h to 21 days, and quantitative autoradiography was used to evaluate cholinergic receptor subtype expression in the cerebral cortex and hippocampus. As previously reported, the alpha7* nAChr was the most sensitive target of TBI-induced plasticity. Significant decreases in alpha-[(125)I]-bungarotoxin (BTX) binding occurred as early as 1 h post-TBI, and persisted in some brain regions for up to 21 days. A kinetic analysis of changes in BTX binding, performed 2 days following brain injury, indicated that the binding deficits are not due to significant changes in receptor affinity. TBI-induced changes in alpha3*/alpha4* nACh receptors, muscarinic cholinergic receptors, and NMDA-type glutamate receptor expression were lower in magnitude, restricted to fewer brain regions and more transient in nature. Persistent deficits in alpha7* nAChr expression following TBI may contribute to impaired functional outcome following brain injury.

Objects referenced in this article
Gene CHRNA3 cholinergic receptor nicotinic alpha 3 subunit Homo sapiens
Gene Chrna3 cholinergic receptor, nicotinic, alpha polypeptide 3 Mus musculus
Gene Chrna3 cholinergic receptor nicotinic alpha 3 subunit Rattus norvegicus

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