Abstract
The effect of increased extracellular calcium on long-term potentiation (LTP) of synaptic transmission has been examined in the CA1 region of guinea pig hippocampal slice preparation using extracellular recordings from the dendritic layer. The application of high calcium (4 mM) led to an increase in the initial slope of the field potential that reserved following return to control (2 mM calcium) solution. The magnitude of the field potential change was unaffected by prior induction of LTP, and inputs tetanized after return to control solution showed the same amount of LTP as those tetanized before the high calcium application. These results suggest that the calcium application by itself did not induce LTP. Inputs tetanized in the high calcium solution showed a greater amount of potentiation than in control solution, any given train producing about twice as much potentiation. However, using long trains (40 impulses) at high strength (2x test strength) gave similar LTP values in the two solutions. The facilitatory effect of high calcium on LTP was completely blocked by raising extracellular magnesium from 2 to 4 mM. As in control solution, LTP evoked in the high calcium solution was blocked by 2-amino-5-phosphono-valerate. The results support the view that calcium influx through postsynaptic N-methyl- d-aspartate receptor channels is directly involved in the induction of LTP.
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