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Closed Access item Activation and desensitization properties of native and recombinant kainate receptors

Authors:Paternain, Ana V.
Rodríguez-Moreno, Antonio
Villarroel, Álvaro
Lerma Gómez, Juan
Keywords:Kainate receptors, Glutamate, Desensitization, Activation, ConA, GluR6 receptor, HEK 293 cells, Hippocampus
Issue Date:1-Oct-1998
Publisher:Elsevier
Citation:Neuropharmacology 37(10-11): 1249-1259 (1998)
Abstract:The activation–inactivation properties of membrane currents induced by the rapid application of glutamate or kainate were studied in cultured hippocampal neurons and in HEK cells transfected with a cDNA encoding the GluR6 subunit. The onset of desensitization was rapid and similar in native and recombinant channels (80 s−1 of onset rate constant). Recovery from desensitization was slow and agonist-dependent in neurons, proceeding slightly faster in GluR6 receptors. Half-maximal activation (EC50) of native channels was obtained at a glutamate concentration of 330 μM, while the half-maximal steady state desensitization (IC1/2) was attained at 2.8 μM. These values differed from those obtained in recombinant receptors (EC50=762 μM and IC1/2=0.44 μM). A small window under the crossing point of activation and inactivation curves was observed, indicating that, for some concentrations of either agonist, steady state channel activity could exist. In native receptors, this window presented maximum values at approximately 100 μM for glutamate, which predicted well the potency of glutamate to reduce the GABAergic drive in hippocampal slices. These data indicate that for neuronal kainate receptors, the concentrations for half activation and half inactivation differ by two orders of magnitude such that the maximum response to a maintained concentration of glutamate is small, and the steady state dose response curve is skewed and bell shaped.
Description:11 páginas, 7 figuras.
Publisher version (URL):http://dx.doi.org/10.1016/S0028-3908(98)00098-7
URI:http://hdl.handle.net/10261/32561
ISSN:0028-3908
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Appears in Collections:(IC) Artículos

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