Glutamate-induced long-term potentiation enhances spontaneous EPSC amplitude but not frequency.
1. Many examples of long-term potentiation (LPT) are induced by repetitive electrical stimulation of presynaptic axons. LTP also is induced by direct glutamate iontophoresis (1 M, 1-2 microA, 10 s) onto postsynaptic neurons in hippocampal slices without evoked presynaptic stimulation; this form of LTP is called "ionto-LTP". The studies herein test the hypothesis that ionto-LTP is expressed primarily through postsynaptic mechanisms. 2. Whole cell recordings were used to examine the amplitude and frequency of spontaneous excitatory postsynaptic currents (sEPSCs) in CA1 pyramidal neurons. sEPSCs were composed of an equal mixture of tetrodotoxin (TTX)-insensitive miniature EPSCs and EPSCs that appeared to result from spontaneous action potentials (i.e., TTX-sensitive EPSCs). The detection of all sEPSCs was virtually eliminated by 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM), suggesting that sEPSCs were glutamate-mediated synaptic events. 3. Changes in the amplitude and frequency of sEPSCs were examined during the expression of ionto-LTP to obtain new information about the cellular location of mechanisms involved in synaptic plasticity. Our findings show that ionto-LTP expression results in increased sEPSC amplitude in the absence of lasting increases in sEPSC frequency. 4. Potentiation of sEPSC amplitude without changes in sEPSC frequency has been previously interpreted to be due to postsynaptic mechanisms. Although this interpretation is supported by findings from peripheral synapses, its application to the central nervous system is unclear. We have considered alternative mechanisms. Models based on increased release probability for action potential dependent transmitter release appeared insufficient to explain our results. The most straightforward interpretation of our results is that LTP induced by glutamate iontophoresis on dendrites of CA1 pyramidal neurons is mediated largely by postsynaptic changes.
Cormier
R J
RJ
Department of Neurobiology and Anatomy, University of Texas Medical School, Houston 77225, USA.
Kelly
P T
PT
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000818:Animals; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000494:pharmacology*; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D007478:Iontophoresis; D017774:Long-Term Potentiation / Q000187:drug effects*; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects*; D013779:Tetrodotoxin / Q000494:pharmacology
D018691:Excitatory Amino Acid Antagonists; D018698:Glutamic Acid; D013779:Tetrodotoxin; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione