Abegg Mathias H, Savic Natasa, Ehrengruber Markus U, McKinney R Anne, Gähwiler Beat H
Brain Research Institute, University of Zurich, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland.
J Physiol. 2004 Jan 15;554(Pt 2):439-48. doi: 10.1113/jphysiol.2003.052662. Epub 2003 Oct 31.
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)-alpha-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.
尽管癫痫发作的特征是过度兴奋,但兴奋性突触传递在癫痫的诱发和发作过程中的作用仍不清楚。在此,我们表明癫痫样活动通过增加CA3-CA1突触中功能性(RS)-α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)型谷氨酸受体的数量来增强海马兴奋性突触。这种形式的突触增强会阻碍长时程增强(LTP)并增强长时程抑制(LTD),而LTP和LTD是与学习和记忆相关的过程。这些突触传递和可塑性的变化可被N-甲基-D-天冬氨酸(NMDA)受体拮抗剂完全阻断,它们可能是癫痫诱发和癫痫发作相关记忆缺陷的基础。