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.
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Translated from Zhurnal Vysshei Nervnoi Deyatel’nosti imeni I. P. Pavlova, Vol. 64, No. 1, pp. 54–63, January–February, 2014.
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Popov, V.A., Markevich, V.A. The Key Role of Calcium in the Mechanism of Deprivation Potentiation of Population Responses of Neurons in Hippocampal Field CA1. Neurosci Behav Physi 45, 483–489 (2015). https://doi.org/10.1007/s11055-015-0099-3
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DOI: https://doi.org/10.1007/s11055-015-0099-3