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Abstract <p>The effect of elevated exogenous interleukin-6 (IL-6) levelson the induction and developmental dynamics of post-tetanic modificationsin response to high-frequency stimulation of the Schaffer collateralswas investigated in the CA1 region of rat hippocampal slices. IL-6exposure was started 10 min before stimulation (to ensure its morespecific action) and stopped 15 min after tetanization (to limitits direct impact on the mechanisms of LTP maintenance). The resultingincrease in the probability of long-term depression (LTD) with alow probability of LTP induction indicates the influence of IL-6on synaptic metaplasticity. Furthermore, IL-6 suppressed post-tetanicshort-term potentiation, suggesting a possible impairment of presynapticplasticity mechanisms. At the same time, a deficit in early LTPdid not prevent the onset of potentiation after IL-6 washout. Theobtained data do not provide grounds to believe that elevated IL-6acts as a negative regulator of the mechanisms of LTP consolidationand maintenance; instead, it may provoke an imbalance between homeostaticand long-term synaptic plasticity.</p>

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Effect of Interleukin-6 on Long-Term Potentiation Induction and Development in Rat Hippocampal Slices

  • 期刊论文

  • 发表日期：

    2025年12月19日

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  • I. V. Kudryashova

摘要

Abstract

The effect of elevated exogenous interleukin-6 (IL-6) levelson the induction and developmental dynamics of post-tetanic modificationsin response to high-frequency stimulation of the Schaffer collateralswas investigated in the CA1 region of rat hippocampal slices. IL-6exposure was started 10 min before stimulation (to ensure its morespecific action) and stopped 15 min after tetanization (to limitits direct impact on the mechanisms of LTP maintenance). The resultingincrease in the probability of long-term depression (LTD) with alow probability of LTP induction indicates the influence of IL-6on synaptic metaplasticity. Furthermore, IL-6 suppressed post-tetanicshort-term potentiation, suggesting a possible impairment of presynapticplasticity mechanisms. At the same time, a deficit in early LTPdid not prevent the onset of potentiation after IL-6 washout. Theobtained data do not provide grounds to believe that elevated IL-6acts as a negative regulator of the mechanisms of LTP consolidationand maintenance; instead, it may provoke an imbalance between homeostaticand long-term synaptic plasticity.