Abstract

Studies using in vitro rat hippocampal slices addressed the mechanism of deprivation potentiation (DeP) of neuron population responses in field CA1 developing as a result of prolonged (60 or 120 min) cessation of rare (0.05 Hz) test stimuli of Schaffer collaterals (SC). The development of DeP was found to involve two independent mechanisms: pre- and postsynaptic, responsible for induction of the short-term and long-term components of DeP, respectively. These studies showed that the interaction of DeP and long-term post-tetanic potentiation (LTP) is competitive in nature, providing evidence of similarity in the mechanisms of the long-term phase of DeP and the phase of LTP associated with protein phosphorylation. Our investigation showed that the Ca2+-dependent mechanism of induction of the postsynaptic component of DeP does not involve NMDA receptors, but does involve purine P2 receptors. A common curve for the relationship between the efficiency of synaptic transmission and the use/non-use of synapses including DeP, long-term depression (LTD), and LTP zones is presented.

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