Epileptiform activity induced metaplasticity impairs bidirectional plasticity in the hippocampal CA1 synapses via GluN2B NMDA receptors

RahumathNasarudeen; AbhinavSingh; Zubin SinghRanaPradeepPunnakkal

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Epileptiform activity induced metaplasticity impairs bidirectional plasticity in the hippocampal CA1 synapses via GluN2B NMDA receptors

机译：Epileptiform activity induced metaplasticity impairs bidirectional plasticity in the hippocampal CA1 synapses via GluN2B NMDA receptors

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Abstract Temporal lobe epilepsy (TLE) is the most common type of epilepsy in humans. Cognitive impairment and memory consolidation problems are common among TLE patients. To understand the changes in the cellular process of memory in TLE, we studied the long-term depression (LTD) in Schaffer-collateral (Sc) CA1 synapses in an epilepsy model. Long-term potentiation (LTP) was investigated in patient samples and animal models by several groups, but LTD was not studied with the same interest in epilepsy research. Here we induced epileptiform activity in rat hippocampal slices using magnesium-free high-potassium (7.5?mM?K?+) artificial cerebrospinal fluid (HK-ACSF) and characterized the LTD in Sc-CA1 synapses. We found that epileptiform activity abolished/impaired LTD and depotentiation in the Sc-CA1 synapses. In control slices, application of NMDA (30?μM for 3?min) induced chemical LTD (c-LTD) in Sc-CA1 synapses, whereas epileptiform?activity induced slices showed slow onset potentiation. Induction of LTD using 1?Hz, 900 pulses yielded a similar outcome as c-LTD. Both forms of LTD were NMDA receptor dependent. In addition, we found that the polarity changes in the synaptic plasticity in epileptiform-induced slices were blocked by GluN2B antagonists ifenprodil and Ro 25–6981. Our data suggest that epileptiform-induced metaplasticity inhibits LTD in Sc-CA1 synapses. We provide new insight into the cellular mechanism of memory formation during epilepsy.

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《Experimental Brain Research》 |2022年第12期|3339-3349|共11页
作者
RahumathNasarudeen; AbhinavSingh; Zubin SinghRanaPradeepPunnakkal;
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作者单位

Division of Molecular Medicine, BMT Wing,Sree Chitra Tirunal Institute for Medical Sciences and;

Department of Biophysics,Postgraduate Institute of Medical Education and Research;

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正文语种英语
中图分类神经病学;
关键词
LTD; Metaplasticity; NMDA receptors; GluN2B; Synaptic plasticity; Temporal lobe epilepsy; Depotentiation;

Epileptiform activity induced metaplasticity impairs bidirectional plasticity in the hippocampal CA1 synapses via GluN2B NMDA receptors

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