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

We investigated a role of calcium in the mechanisms of deprivational potentiation (DeP) of the popspikes amplitude of CAI neurons that was induced in consequence of long (60 min) interruption of rare test stimulation (0.05 Hz) of Schaffer collaterals in rat hippocampal slices. There are two phases of deprivational potentiation that have presumably different genesis: short-term initial "peak" (about 12 min) and long-term "plateau" (more than 1 h). The presence of the membrane permeable Ca2+ chelator (BAPTA-AM) in the solution, or decrease of [Ca2+](out), or depletion of intracellular Ca2+ stores (in the presence of thapsigargin/cyclopiazonic acid) led to reduction of the short-term and to suppression of the long-term phases of DeP. Thus the key role of calcium in the DeP induction mechanisms and participation of two main sources (the extracellular environment and the intracellular Ca2+ stores) was demonstrated.