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Activation of Rho after traumatic brain injury and seizure in rats.
Exp Neurol. 2006 Apr; 198(2):361-9.EN

Abstract

Traumatic brain injury (TBI) is characterized by a progressive cell loss and a lack of axonal regeneration. In the central nervous system (CNS), the Rho signaling pathway regulates the neuronal response to growth inhibitory proteins and regeneration of damaged axons, and Rho activation is also correlated with an increased susceptibility to apoptosis. To evaluate whether traumatic brain injury (TBI) results in changes in Rho activation in vulnerable regions of the brain, GTP-RhoA pull down assays were performed on rat cortical and hippocampal tissue homogenates obtained from 24 h to 3 days following lateral fluid percussion brain injury (FPI). Following FPI, a significantly increased RhoA activation was observed from 24 h to 3 days post-injury in the cortex and by 3 days in the hippocampus ipsilateral to the injury. We also detected activated RhoA in the cortex and hippocampus contralateral to the injury, without concomitant changes in total RhoA levels. To determine if immediate post-traumatic events such as seizures may activate Rho, we examined RhoA activation in the brains of rats with kainic acid-induced seizures. Severe seizures resulted in bilateral RhoA activation in the cortex and hippocampus. Together, these results indicate that RhoA is activated in vulnerable brain regions following traumatic and epileptic insults to the CNS.

Authors+Show Affiliations

Université de Montréal, 2900 Edouard-Montpetit, Faculté de médecine, Département de Pathologie et Biologie cellulaire, Montréal, QC, Canada H3T 1J4.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

16448651

Citation

Dubreuil, Catherine I., et al. "Activation of Rho After Traumatic Brain Injury and Seizure in Rats." Experimental Neurology, vol. 198, no. 2, 2006, pp. 361-9.
Dubreuil CI, Marklund N, Deschamps K, et al. Activation of Rho after traumatic brain injury and seizure in rats. Exp Neurol. 2006;198(2):361-9.
Dubreuil, C. I., Marklund, N., Deschamps, K., McIntosh, T. K., & McKerracher, L. (2006). Activation of Rho after traumatic brain injury and seizure in rats. Experimental Neurology, 198(2), 361-9.
Dubreuil CI, et al. Activation of Rho After Traumatic Brain Injury and Seizure in Rats. Exp Neurol. 2006;198(2):361-9. PubMed PMID: 16448651.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Activation of Rho after traumatic brain injury and seizure in rats. AU - Dubreuil,Catherine I, AU - Marklund,Niklas, AU - Deschamps,Kathleen, AU - McIntosh,Tracy K, AU - McKerracher,Lisa, Y1 - 2006/01/31/ PY - 2005/06/29/received PY - 2005/09/29/revised PY - 2005/12/06/accepted PY - 2006/2/2/pubmed PY - 2006/6/10/medline PY - 2006/2/2/entrez SP - 361 EP - 9 JF - Experimental neurology JO - Exp Neurol VL - 198 IS - 2 N2 - Traumatic brain injury (TBI) is characterized by a progressive cell loss and a lack of axonal regeneration. In the central nervous system (CNS), the Rho signaling pathway regulates the neuronal response to growth inhibitory proteins and regeneration of damaged axons, and Rho activation is also correlated with an increased susceptibility to apoptosis. To evaluate whether traumatic brain injury (TBI) results in changes in Rho activation in vulnerable regions of the brain, GTP-RhoA pull down assays were performed on rat cortical and hippocampal tissue homogenates obtained from 24 h to 3 days following lateral fluid percussion brain injury (FPI). Following FPI, a significantly increased RhoA activation was observed from 24 h to 3 days post-injury in the cortex and by 3 days in the hippocampus ipsilateral to the injury. We also detected activated RhoA in the cortex and hippocampus contralateral to the injury, without concomitant changes in total RhoA levels. To determine if immediate post-traumatic events such as seizures may activate Rho, we examined RhoA activation in the brains of rats with kainic acid-induced seizures. Severe seizures resulted in bilateral RhoA activation in the cortex and hippocampus. Together, these results indicate that RhoA is activated in vulnerable brain regions following traumatic and epileptic insults to the CNS. SN - 0014-4886 UR - https://www.unboundmedicine.com/medline/citation/16448651/Activation_of_Rho_after_traumatic_brain_injury_and_seizure_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(05)00458-9 DB - PRIME DP - Unbound Medicine ER -