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Kainate receptors depress excitatory synaptic transmission at CA3-->CA1 synapses in the hippocampus via a direct presynaptic action

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Item Type:Article
Title:Kainate receptors depress excitatory synaptic transmission at CA3-->CA1 synapses in the hippocampus via a direct presynaptic action
Creators Name:Frerking, M., Schmitz, D., Zhou, Q., Johansen, J. and Nicoll, R.A.
Abstract:Kainate receptor activation depresses synaptic release of neurotransmitter at a number of synapses in the CNS. The mechanism underlying this depression is controversial, and both ionotropic and metabotropic mechanisms have been suggested. We report here that the AMPA/kainate receptor agonists domoate (DA) and kainate (KA) cause a presynaptic depression of glutamatergic transmission at CA3-->CA1 synapses in the hippocampus, which is not blocked by the AMPA receptor antagonist GYKI 53655 but is blocked by the AMPA/KA receptor antagonist CNQX. Neither a blockade of interneuronal discharge nor antagonists of several neuromodulators affect the depression, suggesting that it is not the result of indirect excitation and subsequent release of a neuromodulator. Presynaptic depolarization, achieved via increasing extracellular K(+), caused a depression of the presynaptic fiber volley and an increase in the frequency of miniature EPSCs. Neither effect was observed with DA, suggesting that DA does not depress transmission via a presynaptic depolarization. However, the effects of DA were abolished by the G-protein inhibitors N-ethylmaleimide and pertussis toxin. These results suggest that KA receptor activation depresses synaptic transmission at this synapse via a direct, presynaptic, metabotropic action.
Keywords:Domoate, Kainate, Metabotropic, Presynaptic, Hippocampus, CA1, Animals, Rats
Source:Journal of Neuroscience
ISSN:0270-6474
Publisher:Society for Neuroscience
Volume:21
Number:9
Page Range:2958-2966
Date:1 May 2001
Additional Information:Copyright © 2001 Society for Neuroscience
Official Publication:http://www.jneurosci.org/content/21/9/2958.long
PubMed:View item in PubMed

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