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• W1981362119 abstract "Immediately following fluid-percussion (F-P) brain injury, the hippocampus exhibits a marked increase in its local CMR glc (LCMR glc ; μmol/100 g/min) as determined using [ 14 C]2-deoxy-d-glucose autoradiography. This injury-induced increase in metabolism is followed in 6 h by a subsequent decrease in LCMR glc . These two postinjury metabolic states may be the result of ionic disruptions following trauma via stimulation of glutamategated ion channels. To determine if endogenous glutamate innervation to the CA 1 region of the hippocampus can provide an anatomical basis for this proposed mechanism, it was removed by kainic-acid–induced destruction of CA 3 , and the effect on CA 1 metabolism following concussive injury was studied. Five days before a lateral F-P injury (3.5–4.5 atm), kainic acid (0.5 μg) or vehicle was stereotaxically injected into the left ventricle of 65 rats. Histological inspection indicated that kainic acid produced severe cell loss primarily in the CA 3 region of the hippocampus ipsilateral to the injection. The metabolic results indicated that immediately following injury, animals with an intact hippocampus exhibited an increase in LCMR glc to 84.6 ± 5 within the CA 1 region, representing a 81.5% increase over controls. However, in the CA 3 -lesioned animals, CA 1 showed no evidence of an injury-induced hypermetabolism, with LCMR glc remaining at control levels (51.4 ± 3.9). At 6 h postinjury, the intact hippocampus exhibited a reduction of LCMR glc to rates of 40.7 ± 4.7 within the CA 1 region, representing a 17.9% reduction compared with controls. In contrast, CA 3 -lesioned animals exhibited less of an injury-induced decrease in LCMR glc within the CA 1 region, exhibiting a mean rate of 43.4 ± 4.5, representing only a 12.5% reduction compared with controls. These results indicate that the removal of the CA 3 projection to CA 1 protects the CA 1 cells from the metabolic dysfunction typically seen following injury. This supports our previous work indicating the important role glutamate plays in the ionic flux and subsequent metabolic changes that follow traumatic brain injury." @default.
• W1981362119 created "2016-06-24" @default.
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• W1981362119 date "1992-11-01" @default.
• W1981362119 modified "2023-09-25" @default.
• W1981362119 title "Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁" @default.
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• W1981362119 doi "https://doi.org/10.1038/jcbfm.1992.137" @default.
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