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  • Title: Calcium accumulation by glutamate receptor activation is involved in hippocampal cell damage after ischemia.
    Author: Benveniste H, Jørgensen MB, Diemer NH, Hansen AJ.
    Journal: Acta Neurol Scand; 1988 Dec; 78(6):529-36. PubMed ID: 2906199.
    Abstract:
    Rats exposed to 10 min of complete cerebral ischemia develop necrosis of the CA-1 region of the hippocampus after 2-3 days. We studied the involvement of synaptic transmission for this process by ablation of the afferent input (which is mainly glutamatergic) to CA1 by bilateral destruction of CA-3 neurons (Schafferotomi). The deafferentiation completely prevented the ischemic nerve cell destruction as revealed by histological studies after 6 days. The role of intracellular Ca++ overload was assessed by measurement of the interstitial Ca++ concentration. In control animals the interstitial Ca++ concentration decreases abruptly to 10% of the initial value 1.6 min after the onset of ischemia. The denervated hippocampi, however, showed no decrease during the 10 min of ischemia and hippocampi injected with 2-amino-5-phosphovalerate (APV), a competitive antagonist of the glutamate N-methyl-D-aspartate (NMDA) receptors, displayed a significantly reduced decrease (45% of the initial value) during ischemia. It is concluded that calcium influx via the glutamate-operated channels during the ischemic period is an important link in the development of ischemic brain cell damage.
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