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Am J Physiol Regul Integr Comp Physiol 261: R1527-R1532, 1991;
0363-6119/91 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 6 1527-R1532, Copyright © 1991 by American Physiological Society

ARTICLES

kappa-Opioid antagonist improves cellular bioenergetics and recovery after traumatic brain injury

R. Vink, P. S. Portoghese and A. I. Faden
Department of Chemistry and Biochemistry, James Cook University of North Queensland, Townsville, Australia.

Treatment with opioid receptor antagonists improves outcome after experimental brain trauma, although the mechanisms underlying the protective actions of these compounds remain speculative. We have proposed that endogenous opioids contribute to the pathophysiology of traumatic brain injury through actions at kappa-opioid receptors, possibly by affecting cellular bioenergetic state. In the present study, the effects of the kappa-selective opioid-receptor antagonist nor-binaltorphimine (nor-BNI) were examined after fluid percussion brain injury in rats. Metabolic changes were evaluated by 31P magnetic resonance spectroscopy; the same animals were subsequently followed over 2 wk to evaluate neurological recovery. Nor-BNI, administered intravenously as a 10 or 20 mg/kg bolus at 30 min after injury, significantly improved neurological outcome at 2 wk posttrauma compared with controls. Animals treated with nor-BNI showed significantly greater recovery of intracellular free magnesium concentrations and cytosolic phosphorylation potentials during the first 4 h after injury compared with saline-treated controls. The improvement in cytosolic phosphorylation potential was significantly correlated to neurological outcome. These data support the hypothesis that kappa-opioid receptors mediate pathophysiological changes after traumatic brain injury and that the beneficial effects of opioid-receptor antagonist may result from improvement of posttraumatic cellular bioenergetics.


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J. B. Redell, A. N. Moore, and P. K. Dash
Expression of the Prodynorphin Gene after Experimental Brain Injury and Its Role in Behavioral Dysfunction
Experimental Biology and Medicine, March 1, 2003; 228(3): 261 - 269.
[Abstract] [Full Text] [PDF]


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