In immature rat cerebellar slices, the calcium-dependent increase in cyclic GMP levels provoked by N-methyl-d-aspartic acid (NMDA) (80 μM) displayed sodium dependence using bis-(2-hydroxyethyl)-dimethyl ammonium chloride, N-methyl-glucamine or Tris as sodium substitutes. The effects of NMDA (and also of veratrine, 100 μM) were attenuated by substitution of sodium chloride by lithium chloride. The response produced by depolarization with KCI (50 mM) was not affected by lithium substitution. As lithium is believed to permeate sodium-permeable channels but is not a substrate for sodium/calcium exchange, the data suggest that calcium entry mediated by the reverse mode of sodium/calcium exchange may play a contributory role to the calcium entry provoked by NMDA and veratrine. © 1988.
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