http://purl.uniprot.org/citations/26286172 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/26286172 | http://www.w3.org/2000/01/rdf-schema#comment | "Insulin-like growth factor-1 (IGF-1) is known to promote neurogenesis and survival. However, recent studies have suggested that IGF-1 regulates neuronal firing and excitatory neurotransmission. In the present study, focusing on temporal lobe epilepsy, we found that IGF-1 levels and IGF-1 receptor activation are increased in human epileptogenic tissues, and pilocarpine- and pentylenetetrazole-treated rat models. Using an acute model of seizures, we showed that lateral cerebroventricular infusion of IGF-1 elevates IGF-1 receptor (IGF-1R) signalling before pilocarpine application had proconvulsant effects. In vivo electroencephalogram recordings and power spectrogram analysis of local field potential revealed that IGF-1 promotes epileptiform activities. This effect is diminished by co-application of an IGF-1R inhibitor. In an in vitro electrophysiological study, we demonstrated that IGF-1 enhancement of excitatory neurotransmission and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor- and N-methyl-D-aspartate receptor-mediated currents is inhibited by IGF-1R inhibitor. Finally, activation of extracellular signal-related kinase (ERK)-1/2 and protein kinase B (Akt) in seizures in rats is increased by exogenous IGF-1 and diminished by picropodophyllin. A behavioural study reveals that the ERK1/2 or Akt inhibitor attenuates seizure activity. These results indicate that increased IGF-1 levels after recurrent hippocampal neuronal firings might, in turn, promote seizure activity via IGF-1R-dependent mechanisms. The present study presents a previously unappreciated role of IGF-1R in the development of seizure activity."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.org/dc/terms/identifier | "doi:10.1042/cs20150312"xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/author | "Chen G."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/author | "Gu J."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/author | "Wang X."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/author | "Wang W."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/author | "Wang K."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/author | "Cao Q."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/author | "Jiang G."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/author | "Mi X."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/date | "2015"xsd:gYear |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/name | "Clin Sci (Lond)"xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/pages | "1047-1060"xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/title | "Insulin growth factor-1 (IGF-1) enhances hippocampal excitatory and seizure activity through IGF-1 receptor-mediated mechanisms in the epileptic brain."xsd:string |
http://purl.uniprot.org/citations/26286172 | http://purl.uniprot.org/core/volume | "129"xsd:string |
http://purl.uniprot.org/citations/26286172 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/26286172 |
http://purl.uniprot.org/citations/26286172 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/26286172 |
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