Prolonged activation of NF-kappaB following traumatic brain injury in rats

• Published in: Journal of neurotrauma Vol. 16; no. 11; p. 1023
• Main Authors: Nonaka, M, Chen, X H, Pierce, J E, Leoni, M J, McIntosh, T K, Wolf, J A, Smith, D H
• Format: Journal Article
• Language: English
• Published: United States 01-11-1999
• Subjects: Animals; Brain Injuries - metabolism; Brain Injuries - physiopathology; Endothelium - cytology; Endothelium - metabolism; Male; Mice; Neuroglia - metabolism; Neurons - metabolism; NF-kappa B - metabolism; Rats; Rats, Sprague-Dawley; Time Factors
• ISSN: 0897-7151

Activation of transcription factor, nuclear factor kappa B (NF-kappaB), has been shown to play a key role in inflammatory response, neuronal survival and signaling. We investigated the regional and temporal distribution of activated NF-kappaB in rats at 1 h, 2 h, 24 h, 48 h, 1 week, 2 weeks, 1 month, 2 months, 6 months, and 1 year following brain injury in rats. Early after trauma (1-2 h), activated NF-kappaB was detected in axons, and subsequently found in the cytoplasm and nucleus of neurons by 24 h and lasting up to 1 week. In addition, by 24 h posttrauma, activated NF-kappaB was detected in microglia/macrophages and astrocytes in injured cortex. Surprisingly, this activation persisted for at least 1 year following injury in the cortex, primarily at the margins of progressively enlarging ventricle. Activated NF-kappaB was also detected in endothelial cells, as early as 1 h, and persisted for up to 1 year. These results suggest that a neuronal response to brain trauma includes the activation of NF-kappaB first in the axon with subsequent translocation to the nucleus. Furthermore, these results demonstrate that remarkably prolonged activation of NF-kappaB in glia is found in the same regions undergoing persistent atrophy, suggesting NF-kappaB activation may play a role in long-term inflammatory processes following brain trauma.