Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/4790
DC Field | Value | Language |
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dc.contributor.author | Cunha, Rodrigo A. | - |
dc.contributor.author | Ribeiro, J. A. | - |
dc.contributor.author | Malva, João O. | - |
dc.date.accessioned | 2008-09-01T14:14:31Z | - |
dc.date.available | 2008-09-01T14:14:31Z | - |
dc.date.issued | 2004 | en_US |
dc.identifier.citation | Neurochemistry International. 44:5 (2004) 371-379 | en_US |
dc.identifier.uri | https://hdl.handle.net/10316/4790 | - |
dc.description.abstract | Kainate receptors are ionotropic glutamate receptors located postsynaptically, mediating frequency-dependent transmission, and presynaptically, modulating transmitter release. In contrast to the excitatory postsynaptic kainate receptors, presynaptic kainate receptor can also be inhibitory and their effects may involve a metabotropic action. Arachidonic acid (AA) modulates most ionotropic receptors, in particular postsynaptic kainate receptor-mediated currents. To further explore differences between pre- and postsynaptic kainate receptors, we tested if presynaptic kainate receptors are affected by AA. Kainate (0.3-3 [mu]M) and the kainate receptor agonist, domoate (60-300 nM), inhibited by 19-54% the field excitatory postsynaptic potential (fEPSP) slope in rat CA1 hippocampus, and increased by 12-32% paired-pulse facilitation (PPF). AA (10 [mu]M) attenuated by 37-72% and by 62-66% the domoate (60-300 nM)-induced fEPSP inhibition and paired-pulse facilitation increase, respectively. This inhibition by AA was unaffected by cyclo- and lipo-oxygenase inhibitors, indomethacin (20 [mu]M) and nordihydroguaiaretic acid (NDGA, 50 [mu]M) or by the free radical scavenger, N-acetyl--cysteine (0.5 mM). The K+ (20 mM)-evoked release of [3H]glutamate from superfused hippocampal synaptosomes was inhibited by 18-39% by domoate (1-10 [mu]M), an effect attenuated by 35-63% by AA (10 [mu]M). Finally, the KD (40-55 nM) of the kainate receptor agonist [3H]-(2S,4R)-4-methylglutamate ([3H]MGA) (0.3-120 nM) binding to hippocampal synaptosomal membranes was increased by 151-329% by AA (1-10 [mu]M). These results indicate that AA directly inhibits presynaptic kainate receptor controlling glutamate release in the CA1 area of the rat hippocampus. | en_US |
dc.description.uri | http://www.sciencedirect.com/science/article/B6T0B-49JHH14-1/1/306d6b018d3a5d33b6a0973186ea4ed9 | en_US |
dc.format.mimetype | aplication/PDF | en |
dc.language.iso | eng | eng |
dc.rights | openAccess | eng |
dc.subject | Kainate | en_US |
dc.subject | Arachidonic acid | en_US |
dc.subject | Hippocampus | en_US |
dc.subject | Synaptic transmission | en_US |
dc.subject | Nerve terminals | en_US |
dc.subject | Glutamate release | en_US |
dc.subject | Binding | en_US |
dc.title | Presynaptic kainate receptors modulating glutamatergic transmission in the rat hippocampus are inhibited by arachidonic acid | en_US |
dc.type | article | en_US |
dc.identifier.doi | 10.1016/S0197-0186(03)00167-0 | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.openairetype | article | - |
item.cerifentitytype | Publications | - |
item.grantfulltext | open | - |
item.fulltext | Com Texto completo | - |
item.languageiso639-1 | en | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.researchunit | CNC - Center for Neuroscience and Cell Biology | - |
crisitem.author.orcid | 0000-0003-2550-6422 | - |
crisitem.author.orcid | 0000-0002-5438-4447 | - |
Appears in Collections: | FMUC Medicina - Artigos em Revistas Internacionais |
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file311cfd16de6f4d41a62150aae249ff28.pdf | 174.37 kB | Adobe PDF | View/Open |
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