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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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