Temporal lobe epilepsy is usually associated with cognitive decline and memory deficits. Despite numerous existing studies on various animal models, the mechanisms of these deficits remain largely unclear. A specific form of long-term synaptic efficacy changes-long-term depression (LTD)-is thought to play an important role in memory formation and learning. However, extremely little is known about the possible alteration of LTD induction and dynamics after a status epilepticus (SE). In this work, we investigated the acute and delayed effects of lithium-pilocarpine-induced SE on NMDAR-dependent and NMDAR-independent hippocampal LTD in vitro. We found that SE affected the NMDAR-dependent and NMDAR-independent forms of LTD in different manners. The NMDAR-dependent form of LTD was almost intact 3 days after SE, but it switched from a predominantly presynaptic to a more postsynaptic locus of expression. In contrast, the NMDAR-independent LTD in the hippocampal Schaffer collaterals-CA1 synapses was fully abolished 3 days after SE. Our results emphasize the role of non-NMDA-dependent synaptic plasticity changes in the processes of epileptogenesis and the potential for therapy development.
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