Glutamate release increases during mossy-CA3 LTP but not during Schaffer-CA1 LTP.
Abstract It is still a matter of dispute whether the expression of hippocampal long-term potentiation (LTP) is due to enhanced transmitter release or enhanced postsynaptic sensitivity. Recently we developed a novel method to monitor synaptically released glutamate. In this method, brain slice preparations are stained with a voltage-sensitive dye RH155 which preferentially stains glial cells, and synaptically induced glial depolarization (SIGD) are optically detected in the presence of the blockers for ionotropic glutamate receptors. We have previously shown that SIGD is due to uptake of synaptically released glutamate by glial glutamate transporters. Here we applied this method to examine change in glutamate release during hippocampal LTP. To examine mossy-CA3 LTP, stimulating electrodes were placed in dentate gyrus and tetanic stimulation was delivered in the presence of 50 micro m APV. The amplitude of SIGD after inducing LTP was significantly greater than that in control experiments in which tetanus was not delivered. The amplitude of SIGD after inducing LTP by a brief (3-5 min) application of 50 micro m forskolin was also significantly greater than that in control experiments. At the Schaffer-CA1 synapse, the change in the amplitude of SIGD during LTP induced either by 100 Hz tetanus LTP or 200 Hz tetanus was not significantly greater than that of control experiments. These results provide evidence for increased glutamate release from the presynaptic terminals as the expression mechanism for both tetanus-induced and forskolin-induced LTP at mossy-CA3 synapses, and evidence supporting a postsynaptic expression mechanism at Schaffer-CA1 synapses.
Kawamura
Yoshinobu
Y
Laboratory of Cellular Neurobiology, School of Life Science, Tokyo University of Pharmacy and Life Science, Hachioji, Tokyo 192-0392, Japan.
Manita
Satoshi
S
Nakamura
Takeshi
T
Inoue
Masashi
M
Kudo
Yoshihisa
Y
Miyakawa
Hiroyoshi
H
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D001224:Aspartic Acid / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D005576:Colforsin / Q000494:pharmacology; D004396:Coloring Agents / Q000378:metabolism; D003521:Cyclopropanes / Q000494:pharmacology; D004307:Dose-Response Relationship, Radiation; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D018698:Glutamic Acid / Q000378:metabolism*; D005998:Glycine / Q000031:analogs & derivatives* / Q000494:pharmacology; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D066298:In Vitro Techniques; D007736:Kynurenic Acid / Q000494:pharmacology; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D008274:Magnesium / Q000378:metabolism; D008297:Male; D019599:Mossy Fibers, Hippocampal / Q000502:physiology*; D009457:Neuroglia / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D004396:Coloring Agents; D003521:Cyclopropanes; D018691:Excitatory Amino Acid Antagonists; C120673:benzyloxyaspartate; C082313:2-(2,3-dicarboxycyclopropyl)glycine; D005576:Colforsin; D001224:Aspartic Acid; D018698:Glutamic Acid; D015763:2-Amino-5-phosphonovalerate; D007736:Kynurenic Acid; D008274:Magnesium; D002118:Calcium; D005998:Glycine