Monitoring glutamate release during LTP with glial transporter currents.
Although much has been learned about the mechanisms underlying NMDA receptor-dependent long-term potentiation (LTP), considerable debate remains as to whether LTP is expressed as an increase in the synaptic release of glutamate or as an increase in the sensitivity of the postsynaptic glutamate receptors. We have directly measured changes in the synaptic release of glutamate by recording synaptically evoked glial glutamate transporter currents with whole-cell recording. Glial cell responses were very sensitive to manipulations known to change the release of glutamate yet remained constant during LTP. These results argue strongly for a postsynaptic expression mechanism for LTP.
Lüscher
C
C
Department of Cellular and Molecular Pharmacology, University of California, San Francisco 94143, USA.
Malenka
R C
RC
Nicoll
R A
RA
D000818:Animals; D001692:Biological Transport / Q000502:physiology; D018698:Glutamic Acid / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism*; D066298:In Vitro Techniques; D017774:Long-Term Potentiation; D009457:Neuroglia / Q000502:physiology*; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000502:physiology; D013746:Tetany / Q000503:physiopathology
D018698:Glutamic Acid