Elsevier

Neuroscience Letters

Volume 413, Issue 1, 8 February 2007, Pages 36-41
Neuroscience Letters

Traumatic brain injury stimulates hippocampal catechol-O-methyl transferase expression in microglia

https://doi.org/10.1016/j.neulet.2006.11.060Get rights and content

Abstract

Outcome following traumatic brain injury (TBI) is in large part determined by the combined action of multiple processes. In order to better understand the response of the central nervous system to injury, we utilized an antibody array to simultaneously screen 507 proteins for altered expression in the injured hippocampus, a structure critical for memory formation. Array analysis indicated 41 candidate proteins have altered expression levels 24 h after TBI. Of particular interest was catechol-O-methyl transferase (COMT), an enzyme involved in metabolizing catecholamines released following neuronal activity. Altered catecholamine signaling has been observed after brain injury, and may contribute to the cognitive dysfunctions and behavioral deficits often experienced after TBI. Our data shows that COMT expression in the injured ipsilateral hippocampus was elevated for at least 14 d after controlled cortical impact injury. We found strong co-localization of COMT immunoreactivity with the microglia marker Iba1 near the injury site. Since dopamine transporter expression has been reported to be down-regulated after brain injury, COMT-mediated catecholamine metabolism may play a more prominent role in terminating catecholamine signaling in injured areas.

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Acknowledgements

We would like to thank Melanie Moody and Min Zhang for surgical assistance, Anthony Moore for critical comments, and Dr. Ray Grill for confocal assistance. Research supported by National Institutes of Health grants NS35457, NS049160, and MH072933.

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