Enhanced Phosphodiestric Breakdown of Phosphatidylinositol Bisphosphate After Experimental Brain Injury
Article first published online: 23 NOV 2002
Journal of Neurochemistry
Volume 63, Issue 2, pages 773–776, August 1994
How to Cite
Prasad, M. R., Dhillon, H. S., Carbary, T., Dempsey, R. J. and Scheff, S. W. (1994), Enhanced Phosphodiestric Breakdown of Phosphatidylinositol Bisphosphate After Experimental Brain Injury. Journal of Neurochemistry, 63: 773–776. doi: 10.1046/j.1471-4159.1994.63020773.x
- Issue published online: 23 NOV 2002
- Article first published online: 23 NOV 2002
- Resubmitted manuscript received April 8, 1994; accepted April 25, 1994.
- Brain injury;
- Fluid percussion;
- Inositol phosphates;
Abstract: Regional levels of lactate and inositol 1,4,5-trisphosphate (IP3), a cellular second messenger of the excitatory neurotransmitter system, were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min postinjury, tissue lactate concentrations were significantly elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres. By 20 min postinjury, lactate concentrations were elevated only in the cortices and hippocampus of the ipsilateral hemisphere. Whereas the IP3 concentrations were elevated in the hippocampi of the ipsilateral and contralateral hemisphere and in the cortex of ipsilateral hemisphere at 5 min postinjury, no elevation in these sites was found at 20 min postinjury. Histologic analysis revealed neuronal damage in the cortex and CA3 regions of hippocampus ipsilateral to the injury at 24 h postinjury. The present results suggest activation of the phosphoinositide signal transduction pathway at the onset of injury and of a possible requirement of early persistent metabolic dysfunction (>20 min) such as the lactate accumulation in the delayed neuronal damage.