caa a22 4500 477038212 CHVBK 20180405111310.0 cr unu---uuuuu 170330e19960201xx s 000 0 eng 10.1007/BF02740744 doi (NATIONALLICENCE)springer-10.1007/BF02740744 Ionotropic glutamate receptors [Elektronische Daten] Their possible role in the expression of hippocampal synaptic plasticity [Fredrik Asztély, Bengt Gustafsson] In the brain, most fast excitatory synaptic transmission is mediated through L-glutamate acting on postsynaptic ionotropic glutamate receptors. These receptors are of two kinds—the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate (non-NMDA) and theN-methyl-D-aspartate (NMDA) receptors, which are thought to be colocalized onto the same postsynaptic elements. This excitatory transmission can be modulated both upward and downward, long-term potentiation (LTP) and long-term depression (LTD), respectively. Whether the expression of LTP/LTD is pre-or postsynaptically located (or both) remains an enigma. This article will focus on what postsynaptic modifications of the ionotropic glutamate receptors may possibly underly long-term potentiation/depression. It will discuss the character of LTP/LTD with respect to the temporal characteristics and to the type of changes that appears in the non-NMDA and NMDA receptor-mediated synaptic currents, and what constraints these findings put on the possible expression mechanism(s) for LTP/LTD. It will be submitted that if a modification of the glutamate receptors does underly LTP/LTD, an increase/decrease in the number of functional receptors is the most plausible alternative. This change in receptor number will have to include a coordinated change of both the non-NMDA and the NMDA receptors. Humana Press Inc, 1996 Glutamate receptor channels nationallicence NMDA nationallicence non-NMDA nationallicence synaptic plasticity nationallicence long-term potentiation nationallicence long-term depression nationallicence hippocampus nationallicence Asztély Fredrik Institute of Physiology, Göteborg University, Göteborg, Sweden aut Gustafsson Bengt Institute of Physiology, Göteborg University, Göteborg, Sweden aut Molecular Neurobiology Humana Press 12/1(1996-02-01), 1-11 0893-7648 12:1<1 1996 12 12035 https://doi.org/10.1007/BF02740744 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF02740744 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Asztély Fredrik Institute of Physiology, Göteborg University, Göteborg, Sweden aut NATIONALLICENCE 700 1- Gustafsson Bengt Institute of Physiology, Göteborg University, Göteborg, Sweden aut NATIONALLICENCE 773 0- Molecular Neurobiology Humana Press 12/1(1996-02-01), 1-11 0893-7648 12:1<1 1996 12 12035 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer