Glutamate release monitored with astrocyte transporter currents during LTP.
Long-term potentiation (LTP) of synaptic transmission in the CA1 region of the hippocampus is thought to result from either increased transmitter release, heightened postsynaptic sensitivity, or a combination of the two. We have measured evoked glutamate release from Schaffer collateral/commissural fiber terminals in CA1 by recording synaptically activated glutamate transporter currents in hippocampal astrocytes located in stratum radiatum. Although several manipulations of release probability caused parallel changes in extracellular field potentials and synaptically activated transporter current amplitudes, induction of LTP failed to alter transporter-mediated responses, suggesting that LTP does not alter the amount of glutamate released upon synaptic stimulation.
Diamond
J S
JS
Vollum Institute, Oregon Health Sciences University, Portland 97201, USA.
Bergles
D E
DE
Jahr
C E
CE
D000818:Animals; D001253:Astrocytes / Q000502:physiology*; D001692:Biological Transport / Q000502:physiology; D019706:Excitatory Postsynaptic Potentials; D018698:Glutamic Acid / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism*; D066298:In Vitro Techniques; D017774:Long-Term Potentiation; D009411:Nerve Endings / Q000378:metabolism; D009412:Nerve Fibers / Q000378:metabolism; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D009435:Synaptic Transmission / Q000502:physiology*
D018698:Glutamic Acid