Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/21501
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dc.date.accessioned2021-08-20T12:26:30Z-
dc.date.available2021-08-20T12:26:30Z-
dc.date.issued1997-
dc.identifier.citationBüyükuysal, L. (1997). "Effect of nitric oxide donors on endogenous dopamine release from rat striatal slices - II: The role of voltage-dependent sodium channels, calcium channel activation, reverse transport mechanism, guanylate cyclase and endogenous glutamate". Fundamental & Clinical Pharmacology, 11(6), 528-536.en_US
dc.identifier.issn0767-3981-
dc.identifier.urihttps://doi.org/10.1111/j.1472-8206.1997.tb00857.x-
dc.identifier.urihttps://onlinelibrary.wiley.com/doi/10.1111/j.1472-8206.1997.tb00857.x-
dc.identifier.urihttp://hdl.handle.net/11452/21501-
dc.description.abstractIncubation of striatal slices with sodium nitroprusside (SNP) or hydroxylamine (HA) for 60 min caused a dose-dependent increase in dopamine (DA) release. This effect was inhibited completely by tetrodotoxin (TTX) (1 mu M) if low concentrations of SNP (1 mu M) or HA (10 and 100 mu M) were tested. Although higher concentration of SNP (10 and 100 mu M) and HA (500 mu M) were still effective in stimulating DA release, increases observed under these conditions were less than the values found in the absence of TTX. Verapamil (10 mu M), but not omega-conotoxin (100 mu M), significantly reduced DA release stimulated by high concentrations of SNP or HA. When verapamil was combined with TTX, moreover, SNP and HA failed to stimulate DA release. If striatal slices were incubated in the presence of nomifensine (10 mu M), SNP and HA did not enhance DA release. SNP and HA-induced depletions in tissue DA levels were also protected by nomifensine. Inhibition of guanylate cyclase with 10 mu M of methylene blue could not reduce the effects of NO-donors. SNP and HA also failed to alter endogenous glutamate release from striatal slices. Similarly, SNP and HA-induced increases in DA release were not affected by kynurenic acid and MK-801. These results indicate that NO-donors SNP and HA stimulate DA release by facilitating reverse DA transport. ?his effect seems to be dependent on the activation of both voltage dependent sodium channels and L-type of calcium channels. Results presented here also indicate that neither endogenous glutamate nor guanylate cyclase activation plays an intermediary role in stimulatory effects of NO-donors on DA release from rat striatal slices.en_US
dc.language.isoenen_US
dc.publisherEditions Scientifiques Medicales Elsevieren_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectPharmacology & pharmacyen_US
dc.subjectDopamine releaseen_US
dc.subjectNitric oxideen_US
dc.subjectReverse transporten_US
dc.subjectGlutamateen_US
dc.subjectCalcium channelsen_US
dc.subjectSodium channelsen_US
dc.subjectGuanylate cyclaseen_US
dc.subjectH-3 norepinephrine releaseen_US
dc.subjectIn-vivo microdialysisen_US
dc.subjectCyclic-GMPen_US
dc.subjectMessengeren_US
dc.subjectBrainen_US
dc.subjectAciden_US
dc.subjectNeurotransmitteren_US
dc.subjectCatecholaminesen_US
dc.subjectNitroprusside modulationen_US
dc.titleEffect of nitric oxide donors on endogenous dopamine release from rat striatal slices - II: The role of voltage-dependent sodium channels, calcium channel activation, reverse transport mechanism, guanylate cyclase and endogenous glutamateen_US
dc.typeArticleen_US
dc.identifier.wos000073018700006tr_TR
dc.identifier.scopus2-s2.0-0346922940tr_TR
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.tr_TR
dc.identifier.startpage528tr_TR
dc.identifier.endpage536tr_TR
dc.identifier.volume11tr_TR
dc.identifier.issue6tr_TR
dc.relation.journalFundamental & Clinical Pharmacologyen_US
dc.contributor.buuauthorBüyükuysal, Levent-
dc.contributor.researcheridAAH-1657-2021tr_TR
dc.identifier.pubmed9444520tr_TR
dc.subject.wosPharmacology & pharmacyen_US
dc.indexed.wosSCIEen_US
dc.indexed.scopusScopusen_US
dc.indexed.pubmedPubmeden_US
dc.contributor.scopusid6602686612tr_TR
dc.subject.scopusNeuronal Nitric Oxide Synthase; 7-Nitroindazole; Pentetrazoleen_US
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