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Epileptiform activity in rat hippocampus strengthens excitatory synapses
Author(s) -
Abegg Mathias H.,
Savic Nataŝa,
Ehrengruber Markus U.,
McKinney R. Anne,
Gähwiler Beat H.
Publication year - 2004
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2003.052662
Subject(s) - long term potentiation , neuroscience , excitatory postsynaptic potential , synaptic plasticity , long term depression , metaplasticity , nmda receptor , hippocampus , ampa receptor , neurotransmission , glutamate receptor , synaptic fatigue , hippocampal formation , epilepsy , neuronal memory allocation , chemistry , biology , inhibitory postsynaptic potential , receptor , biochemistry
Although epileptic seizures are characterized by excessive excitation, the role of excitatory synaptic transmission in the induction and expression of epilepsy remains unclear. Here, we show that epileptiform activity strengthens excitatory hippocampal synapses by increasing the number of functional (RS)‐α‐amino‐3hydroxy‐5methyl‐4‐isoxadepropionate (AMPA)‐type glutamate receptors in CA3–CA1 synapses. This form of synaptic strengthening occludes long‐term potentiation (LTP) and enhances long‐term depression (LTD), processes involved in learning and memory. These changes in synaptic transmission and plasticity, which are fully blocked with N ‐methyl‐D‐aspartate (NMDA) receptor antagonists, may underlie epilepsy induction and seizure‐associated memory deficits.