Browsing by Author "Prasad, M.R."

Now showing 1 - 3 of 3

Alterations in Protein Kinase C activity after experimental brain injury
(Brain Research, 1996) Jayawardena, B.M.; Mark, R.; Dhillon, H.S.; Mattson, M.P.; Prasad, M.R.
Changes in 1,4,5 inositol triphosphate receptors following experimental brain injury
(Neuroscience research communications, 1995) Jayawardena, B.M.; Dhillon, H.S.; Carbary, T.; Prasad, M.R.
Inositol 1,4,5-tris phosphate (IP3), a cellular second messenger of excitatory neurotransmitter system, by interacting with membrane IP3 receptor can mobilize calcium from internal stores. Regional binding properties of IP3 receptor were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min postinjury, a significant decrease in the IP3 receptor density was found only in the ipsilateral left hippocampus. At 20 min after injury, significant decreases were observed in both the receptor density and the half maximal reduction of IP3, binding in both the injured left cortex and ipsilateral hippocampus. These findings suggest that increases of ligand affinity to the IP3 receptor after brain injury. This change in the IP3 receptor in concert with the increased IP3 (21) may facilitate a possible IP3 action of calcium mobilization in the brain regions that undergo neuronal cell loss after brain injury.
Regional Concentrations of Cyclic Nucleotides After Experimental Brain Injury
(Journal of Neurotrauma, 1995) Dhillon, H.S.; Yang, L.; Jayawardena, B.M.; Dempsey, R.J.; Prasad, M.R.
Regional concentrations of lactate, glucose, cAMP, and cGMP were measured after lateral fluid percussion brain injury in rats. At 5 min after injury, while tissue concentrations of lactate were elevated in the cortices and hippocampi of both the ipsilateral and contralateral hemispheres, those of glucose were decreased in these brain regions. By 20 min after injury, increases of lactate concentrations and decreases of glucose concentrations were observed only in the cortices and in the hippocampus of the ipsilateral hemisphere. Whereas the cAMP concentrations were unchanged in the cortices and hippocampi of the ipsilateral and contralateral hemispheres at 5 min after injury, decreases were found in the injured cortex and ipsilateral hippocampus at 20 min after injury. The tissue concentrations of cGMP were found to be elevated only in the ipsilateral hippocampus at 5 min after injury. The present observation that tissue glucose decreases in the injured cortex and the ipsilateral hippocampus are consistent with the published findings of increased hyperglycolysis and oxidative metabolism in brain immediately after injury. The present findings that the concentrations of cAMP and cGMP change in the cortex and hippocampus provide biochemical evidence for the neurotransmitter's surge after brain injury.