The Key Role of Calcium in the Mechanism of Deprivation Potentiation of Population Responses of Neurons in Hippocampal Field CA1

Abstract

In vitro studies on living rat hippocampus slices addressed the role of Ca2+ in the mechanism of deprivation potentiation of population responses (pop spikes) of neurons in field CA1 induced by prolonged (60 min) interruption of low-frequency test stimulation of Schaffer collaterals. Two phases were seen in deprivation potentiation, with presumptively different origins: an initial short-lived “peak” (about 12 min) and a longer-lasting “plateau” (more than 1 h). The experiments reported here showed that the presence of a penetrating Ca2+ chelator (BAPTA-AM), decreasing the Ca2+ concentration in the solution, and depletion of the intracellular calcium depot (presence of thapsigargin/cyclopiazonic acid in the solution) led to reductions in the transient phase and blockade of the longer-lasting phase of deprivation potentiation. These studies thus demonstrate the key roles of both extracellular and stored intracellular calcium in the mechanism of development of deprivation potentiation.