{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T07:25:35Z","timestamp":1790666735156,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2013,4,25]],"date-time":"2013-04-25T00:00:00Z","timestamp":1366848000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Traffic"],"published-print":{"date-parts":[[2013,7]]},"abstract":"<jats:p><jats:bold>Kainate receptors (<jats:styled-content style=\"fixed-case\">KARs<\/jats:styled-content>) play fundamentally important roles in controlling synaptic function and regulating neuronal excitability. Postsynaptic <jats:styled-content style=\"fixed-case\">KARs<\/jats:styled-content> contribute to excitatory neurotransmission but the molecular mechanisms underlying their activity\u2010dependent surface expression are not well understood. Strong activation of <jats:styled-content style=\"fixed-case\">KARs<\/jats:styled-content> in cultured hippocampal neurons leads to the downregulation of postsynaptic <jats:styled-content style=\"fixed-case\">KARs<\/jats:styled-content> via endocytosis and degradation. In contrast, low\u2010level activation augments postsynaptic <jats:styled-content style=\"fixed-case\">KAR<\/jats:styled-content> surface expression. Here, we show that this increase in <jats:styled-content style=\"fixed-case\">KARs<\/jats:styled-content> is due to enhanced recycling via the recruitment of Rab11\u2010dependent, transferrin\u2010positive endosomes into spines. Dominant\u2010negative Rab11 or the recycling inhibitor primaquine prevents the kainate\u2010evoked increase in surface <jats:styled-content style=\"fixed-case\">KARs<\/jats:styled-content>. Moreover, we show that the increase in surface expression is mediated via a metabotropic <jats:styled-content style=\"fixed-case\">KAR<\/jats:styled-content> signalling pathway, which is blocked by the protein kinase C inhibitor chelerythrine, the calcium chelator <jats:styled-content style=\"fixed-case\">BAPTA<\/jats:styled-content> and the G\u2010protein inhibitor pertussis toxin. Thus, we report a previously uncharacterized positive feedback system that increases postsynaptic <jats:styled-content style=\"fixed-case\">KARs<\/jats:styled-content> in response to low\u2010 or moderate\u2010level agonist activation and can provide additional flexibility to synaptic regulation.<\/jats:bold><\/jats:p><jats:p><jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/tra12071-gra-0001.gif\" xlink:title=\"image\"\/><\/jats:p>","DOI":"10.1111\/tra.12071","type":"journal-article","created":{"date-parts":[[2013,4,4]],"date-time":"2013-04-04T15:06:18Z","timestamp":1365087978000},"page":"810-822","source":"Crossref","is-referenced-by-count":23,"title":["Postsynaptic Kainate Receptor Recycling and Surface Expression Are Regulated by Metabotropic Autoreceptor Signalling"],"prefix":"10.1111","volume":"14","author":[{"given":"Inmaculada M.","family":"Gonz\u00e1lez\u2010Gonz\u00e1lez","sequence":"first","affiliation":[{"name":"School of Biochemistry University of Bristol  Medical Sciences Building, University Walk Bristol BS8 1TD UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeremy M.","family":"Henley","sequence":"additional","affiliation":[{"name":"School of Biochemistry University of Bristol  Medical Sciences Building, University Walk Bristol BS8 1TD 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