<> <http://www.w3.org/2000/01/rdf-schema#comment> "The repository administrator has not yet configured an RDF license."^^<http://www.w3.org/2001/XMLSchema#string> . <> <http://xmlns.com/foaf/0.1/primaryTopic> <https://discovery.ucl.ac.uk/id/eprint/1306769> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://purl.org/ontology/bibo/Thesis> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://purl.org/ontology/bibo/Article> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/dc/terms/title> "Ca2+ dependent activation of extracellular signal regulated\r\nkinases 1 and 2: role of intrasynaptosomal Ca2+ stores"^^<http://www.w3.org/2001/XMLSchema#string> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/ontology/bibo/abstract> "The aim of the thesis was to examine how Ca2+ activates the ERK pathway and the\r\ncontribution of Ca2+ released from intracellular stores in physiological and\r\npathophysiological conditions using isolated nerve terminals (synaptosomes) in a\r\npresynaptic model. The Ca2+-dependent phosphorylation/activation of ERK1 and ERK2\r\nstimulated by depolarisation of the plasma membrane or by Ca2+ influx mediated by the\r\nionophore ionomycin was significantly reduced by the removal of external Ca2+.\r\nIntrasynaptosomal Ca2+ contribution to the Ca2+-dependent component of ERK1 and\r\nERK2 phosphorylation/activation was indicated by the depletion of intrasynaptosomal\r\nCa2+ or inhibition of the smooth endoplasmic reticulum Ca2+-ATPase pump. Two main\r\npathways were found to lead to the release of Ca2+ from intrasynaptosomal stores.\r\nFirstly, external Ca2+ influx directly activated ryanodine receptors (RyRs) to mediate\r\nCa2+-induced Ca2+ release (CICR). Secondly, Ca2+ influx or activation of GPCRs\r\ncoupled to Gq/11 activated phospholipase C (PLC) to effect PIP2 metabolism and IP3\r\nproduction, with consequent activation of IP3-induced Ca2+ release (IPCR). The\r\nactivation of group I metabotropic glutamate receptor (mGluR1/5) stimulation\r\nsupported IPCR. Intriguingly, inhibition of Ca2+ influx through voltage-dependent\r\ncalcium channels (VDCCs) by stimulating GABAB, group III mGluRs, 5-HT1A and A1\r\nreceptors was suppressed by prior depletion of the smooth endoplasmic reticulum.\r\nMitochondria and acidic compartments also appear to store Ca2+ intrasynaptosomally,\r\nwith mitochondrial depolarisation resulting in a transient increase in ERK1 and ERK2\r\nphosphorylation/activation. Finally, a pathophysiological model of nerve terminal\r\nischemia showed that intrasynaptosomal Ca2+ release contributes to the Ca2+-dependent\r\ncomponent of phosphorylation/activation of ERK1 and ERK2 occurring when Na+/K+-\r\nATPase is inhibited. In conclusion, extracellular Ca2+ influx and intracellular Ca2+ store\r\nrelease together support Ca2+ mediated stimulation of the ERK pathway in synaptosomes. This has important implications in the cross-talk of signalling pathways\r\nto ERK1 and ERK2 phosphorylation/activation and neurotransmitter release from nerve\r\nterminals in physiological and pathophysiological conditions."^^<http://www.w3.org/2001/XMLSchema#string> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/dc/terms/date> "2011-03-28" . <https://discovery.ucl.ac.uk/id/document/26964> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://purl.org/ontology/bibo/Document> . <https://discovery.ucl.ac.uk/id/org/ext-a64c3df5861c6582807add1abaadf2af> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://xmlns.com/foaf/0.1/Organization> . <https://discovery.ucl.ac.uk/id/org/ext-a64c3df5861c6582807add1abaadf2af> <http://xmlns.com/foaf/0.1/name> "UCL (University College London)"^^<http://www.w3.org/2001/XMLSchema#string> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/dc/terms/issuer> <https://discovery.ucl.ac.uk/id/org/ext-a64c3df5861c6582807add1abaadf2af> . <https://discovery.ucl.ac.uk/id/org/ext-3baac1736e17d0191748980b1fccf550> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://xmlns.com/foaf/0.1/Organization> . <https://discovery.ucl.ac.uk/id/org/ext-3baac1736e17d0191748980b1fccf550> <http://xmlns.com/foaf/0.1/name> "Department of Neuroscience, Physiology and Pharmacology, UCL (University College London)"^^<http://www.w3.org/2001/XMLSchema#string> . <https://discovery.ucl.ac.uk/id/org/ext-3baac1736e17d0191748980b1fccf550> <http://purl.org/dc/terms/isPartOf> <https://discovery.ucl.ac.uk/id/org/ext-a64c3df5861c6582807add1abaadf2af> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/dc/terms/issuer> <https://discovery.ucl.ac.uk/id/org/ext-3baac1736e17d0191748980b1fccf550> . <https://discovery.ucl.ac.uk/id/org/ext-a64c3df5861c6582807add1abaadf2af> <http://purl.org/dc/terms/hasPart> <https://discovery.ucl.ac.uk/id/org/ext-3baac1736e17d0191748980b1fccf550> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/ontology/bibo/status> <http://purl.org/ontology/bibo/status/unpublished> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/dc/terms/creator> <https://discovery.ucl.ac.uk/id/person/ext-06ce749a30a02a1b58cd99dd72d3f5ed> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/ontology/bibo/authorList> <https://discovery.ucl.ac.uk/id/eprint/1306769#authors> . <https://discovery.ucl.ac.uk/id/eprint/1306769#authors> <http://www.w3.org/1999/02/22-rdf-syntax-ns#_1> <https://discovery.ucl.ac.uk/id/person/ext-06ce749a30a02a1b58cd99dd72d3f5ed> . <https://discovery.ucl.ac.uk/id/person/ext-06ce749a30a02a1b58cd99dd72d3f5ed> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://xmlns.com/foaf/0.1/Person> . <https://discovery.ucl.ac.uk/id/person/ext-06ce749a30a02a1b58cd99dd72d3f5ed> <http://xmlns.com/foaf/0.1/givenName> "S."^^<http://www.w3.org/2001/XMLSchema#string> . <https://discovery.ucl.ac.uk/id/person/ext-06ce749a30a02a1b58cd99dd72d3f5ed> <http://xmlns.com/foaf/0.1/familyName> "Nizami"^^<http://www.w3.org/2001/XMLSchema#string> . <https://discovery.ucl.ac.uk/id/person/ext-06ce749a30a02a1b58cd99dd72d3f5ed> <http://xmlns.com/foaf/0.1/name> "S. Nizami"^^<http://www.w3.org/2001/XMLSchema#string> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://eprints.org/ontology/EPrint> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://eprints.org/ontology/ThesisEPrint> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://purl.org/dc/terms/isPartOf> <https://discovery.ucl.ac.uk/id/repository> . <https://discovery.ucl.ac.uk/id/eprint/1306769> <http://eprints.org/ontology/hasDocument> <https://discovery.ucl.ac.uk/id/document/26964> . <https://discovery.ucl.ac.uk/id/document/26964> <http://www.w3.org/1999/02/22-rdf-syntax-ns#type> <http://eprints.org/ontology/Document> . <https://discovery.ucl.ac.uk/id/document/26964> <http://www.w3.org/2000/01/rdf-schema#label> "Ca2+ dependent activation of extracellular signal regulated\r\nkinases 1 and 2: role of intrasynaptosomal Ca2+ stores 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