Abstract

Long-lasting potentiation can be induced in area CA1 of hippocampus by a relatively brief (7–10 min) exposure to a higher (4.0 mM) than normal (2.0 mM) extracellular calcium concentration 18,19,38,43,49. We have found that long-lasting calcium-induced potentiation is dependent on extracellular potassium concentration. Slices exposed to high extracellular calcium-in the presence of normal extracellular potassium (3.35 mM) showed a transient facilitation. Long-lasting potentiation was induced by exposure to high calcium only in slices also exposed to higher than normal extracellular potassium (6.25 mM). In intracellular experiments we found that injection of depolarizing current into postsynaptic neurons could substitute for high extracellular potassium. These results suggest that calcium-induced potentiation involves a postsynaptic, voltage-dependent mechanism. A similar conclusion has been reached for tetanus-induced potentiation 9,10,20,35. We also found that calcium-induced potentiation, like tetanus-induced potentiation, is not accompanied by an increase in postsynaptic input resistance.

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