{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T02:47:48Z","timestamp":1779245268728,"version":"3.51.4"},"reference-count":35,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"5007","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[1991,5,10]]},"abstract":"<jats:p>\n            NMDA (\n            <jats:italic>N<\/jats:italic>\n            -methyl -D-aspartate) receptors and non-NMDA receptors represent the two major classes of ion channel-linked glutamate receptors. Unlike the NMDA receptor channels, non-NMDA receptor channels have usually been thought to conduct monovalent cations only. Non-NMDA receptor ion channels that can be gated by kainic acid (KA) and \u03b1-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) are formed by the glutamate receptor subunits GluR1, GluR2, and GluR3. These subunits were expressed in various combinations in\n            <jats:italic>Xenopus<\/jats:italic>\n            oocytes so that their permeability to divalent cations could be studied. At physiological resting potentials, KA and AMPA elicited inward calcium currents in oocytes expressing GluR1, GluR3, and GluR1 plus GluR3. In contrast, oocytes expressing GluR1 plus GluR2 or GluR3 plus GluR2 showed no such permeability. Thus, in neurons expressing certain KA-AMPA receptor subunits, glutamate may trigger calcium-dependent intracellular events by activating non-NMDA receptors.\n          <\/jats:p>","DOI":"10.1126\/science.1709304","type":"journal-article","created":{"date-parts":[[2006,10,5]],"date-time":"2006-10-05T22:10:16Z","timestamp":1160086216000},"page":"851-853","source":"Crossref","is-referenced-by-count":1189,"title":["Ca2\n            <sup>+<\/sup>\n            Permeability of KA-AMPA\u2014Gated Glutamate Receptor Channels Depends on Subunit Composition"],"prefix":"10.1126","volume":"252","author":[{"given":"Michael","family":"Hollmann","sequence":"first","affiliation":[{"name":"Molecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Melissa","family":"Hartley","sequence":"additional","affiliation":[{"name":"Molecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephen","family":"Heinemann","sequence":"additional","affiliation":[{"name":"Molecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92037."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"221","reference":[{"key":"e_1_2_1_1_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1988.sp017077"},{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1988.sp017078"},{"key":"e_1_2_1_3_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1983.sp014852"},{"key":"e_1_2_1_4_1","doi-asserted-by":"crossref","first-page":"583","DOI":"10.1016\/0896-6273(90)90213-Y","volume":"5","year":"1990","unstructured":"BETTLER, B, CLONING OF A NOVEL GLUTAMATE RECEPTOR SUBUNIT, GLUR5 - 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