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The Journal of Neuroscience, May 1, 2001, 21(9):2958-2966

Kainate Receptors Depress Excitatory Synaptic Transmission at CA3CA1 Synapses in the Hippocampus via a Direct Presynaptic Action

Matthew Frerking¹, Dietmar Schmitz¹, Qiang Zhou¹, Joshua Johansen², and Roger A. Nicoll^{1, 2}

Departments of ¹ Cellular and Molecular Pharmacology and ² Physiology, University of California, San Francisco, California 94143-0450

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 CA3CA1 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.

Key words: domoate; kainate; metabotropic; presynaptic; hippocampus; CA1

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Copyright © 2001 Society for Neuroscience  0270-6474/01/2192958-09$05.00/0

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