Kainate receptors and synaptic plasticity

R. A. Nicoll (), J. Mellor, M. Frerking and D. Schmitz
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R. A. Nicoll: Department of Cellular and Molecular Pharmacology University of California
J. Mellor: Department of Cellular and Molecular Pharmacology University of California
M. Frerking: Department of Cellular and Molecular Pharmacology University of California
D. Schmitz: Department of Cellular and Molecular Pharmacology University of California

Nature, 2000, vol. 406, issue 6799, 957-957

Abstract: Abstract Bortolotto et al.1 report that the kainate subtype of glutamate receptor is essential for the plasticity of certain types of synaptic transmission in the brain, which is of interest as these receptors were previously not thought to initiate plastic processes. In particular, a new antagonist (LY382884) was shown to act selectively against the GluR5 type of kainate receptor: in the presence of LY382884, which reduces kainate-receptor-mediated postsynaptic responses by ∼40%, long-term potentiation (LTP) at hippocampal mossy-fibre synapses could no longer be induced1. Here we argue that the available evidence does not support a major role for kainate receptors in the induction of mossy-fibre LTP.

Date: 2000
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DOI: 10.1038/35023075

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