Involvement of Pannexin-1 in the Mechanism of Deprivation Potentiation of Population Spikes of Neurons in Rat Hippocampa
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Involvement of Pannexin-1 in the Mechanism of Deprivation Potentiation of Population Spikes of Neurons in Rat Hippocampal Field CA1 V. A. Popov
UDC 612.822.3
Translated from Zhurnal Vysshei Nervnoi Deyatel’nosti imeni I. P. Pavlova, Vol. 70, No. 3, pp. 360–374, May–June, 2020. Original article submitted July 31, 2019. Revised version received November 8, 2019. Accepted December 16, 2019. Testing of the connections of Schaffer collaterals with field CA1 neurons in living slices of rat hippocampus was used to study the mechanism of deprivation potentiation (DeP) of population spikes developing as a result of a 60-min pause in stimulation (deprivation). Previous studies have shown that DeP has the property of input specificity and the ability to persist for prolonged periods; it consists of two components with independent mechanisms of induction: an initial short-term “peak” of presynaptic origin and a long-lasting “plateau” with a Ca2+-dependent postsynaptic mechanism mediated by P2 purine receptors. Studies of the properties of the input specificity of DeP were run using stimulation of two different populations of Schaffer collaterals and recording of pop-spikes in the general population of neurons in field CA1. These experiments showed that changes in synaptic efficiency in the deprived input depend only on a presynaptic mechanism responsible for the development of the short-term component of DeP. Studies of the postsynaptic mechanism of induction of the long-term component of DeP demonstrated that the function of the adenosine triphosphate (ATP) source required for activation of P2 purine receptors is mediated by pannexin-1, which forms ATP-conducting channels on the postsynapse. A working model of the cyclic mechanism of induction of the long-term component of DeP is presented. Keywords: deprivation potentiation, hippocampal slices, pop spike, input specificity, P2 purine receptors, pannexin-1, probenecid, carbenoxolone.
Along with long-term posttetanic potentiation (LTP) [Bliss and Lømo, 1973] and long-term depression [Lynch et al., 1977], DeP is a variant of synaptic plasticity associated with changes in the nature of afferentation [Popov, 2016]. Previous experiments on living rat hippocampal slices with testing of the connections of Schaffer collaterals with neurons in field CA1 showed that prolonged (from 10 min to 4 h) pauses in the delivery of rare (0.05 Hz) test stimuli lead to the induction of DeP – an increase in the amplitude of population excitatory postsynaptic potentials and, to a greater extent, population spikes (PS), proportional to the duration of the pause (deprivation). Studies demonstrated
that DeP has the property of input specificity and the ability to persist for long periods and that the mechanism of development of DeP may consist of a competitive interaction with the mechanism of development of the late protein kinase C (PKC)-dependent phase of LTP. Two components were identified at the stage of persisting DeP: a short-term component (stDeP) lasting 10–12 min, with a presynaptic mecha
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