The plasticity of inhibitory resposes during CA3-CA1 long-term potentiation (LTP) in the rat hippocampal slices was studied by the method of paired-pulse stimulation. Coefficients of inhibition were estimated by the differences between IPSP dependent and independent paired-pulse plasticity. In the experimental group high frequency stimulation of Schaffer collaterals was delivered under jasplakinolide exposure, this inhibitor of actin depolymerization is used also as activator of actin polymerization. It was shown that the feature of LTP development after induction with blockade of actin depolymerization include altered modification profile of inhibition, specifically involved in resposes to paired-pulse stimulation. Initial enhancement of inhibition depended on the value before tetanization. Therefore this factor may be responsible for between-group differences and it was taken into account in the evaluation of specific for posttetanic depolymerization changes. In result, this phase is related to disinhibition disorder during LTP consolidation and maintenance. It may be assumed that coordinating role of actin cytoskeleton is essential for balanced modifications of excitatory and inhibitory transmission during long-term plasticity.
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