Abstract
The effects of various calcium antagonists, acting at the different neuronal calcium channels, were studied towards two models of in vitro neuronal injury in rat hippocampal slices. In particular, the influence of the drugs were tested on the electrical failure induced by treatment of hippocampal slices with hypoxia or high concentrations of the excitatory amino acid N-methyl-D-aspartate (NMDA). The L-type calcium antagonists, nifedipine (100 μM) and diltiazem (100 μM) or the T-type calcium antagonist amiloride (100 μM) failed to significantly affect the recovery from the CA1 electrical failure induced by both hypoxia or NMDA (50 μM). The N-type calcium antagonists, omega-conotoxin GVIA (0.5 μM) and neomycin (300 μM) significantly (P<0.01) increased the probability of the recovery of the CA1 population spike after hypoxia but not after NMDA (50 μM). The glutamate antagonist dizocilpine (50 μM), tested for comparison, significantly (P<0.01) increased the probability of the recovery of the CA1 population spike after hypoxia and NMDA (50 μM). The results suggest an involvement of calcium channels especially of N-type in the genesis of hypoxic but not NMDA neuronal injury.
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