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dc.creatorAlvarez-Leefmans, F.J.
dc.creatorGamiño, S.M.
dc.creatorGiraldez, F.
dc.creatorNogueron, Isabel
dc.date.accessioned2017-06-29T04:13:59Z
dc.date.available2017-06-29T04:13:59Z
dc.date.issued1988es_ES
dc.identifier65es_ES
dc.identifier.issn0022-3751es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4760
dc.identifier.urihttps://doi.org/10.1113/jphysiol.1988.sp017378es_ES
dc.identifier.urihttps://pubmed.ncbi.nlm.nih.gov/3254412/es_ES
dc.language.isoenges_ES
dc.relation406 (1) 246-255 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleIntracellular chloride regulation in amphibian dorsal root ganglion neurones studied with ion-selective microelectrodeses_ES
dc.typearticlees_ES
dc.contributor.affiliationDepartamento de Farmacología y Toxicología, Centro de Investigación y Estudios Avanzados del IPN, Apartado Postal 14470, México 07000, D.F.es_ES
dc.relation.jnabreviadoJ PHYSIOLes_ES
dc.relation.journalJournal of Physiologyes_ES
dc.identifier.placeLondreses_ES
dc.date.published1988es_ES
dc.identifier.organizacionInstituto Mexicano de Psiquiatríaes_ES
dc.identifier.eissn1469-7793es_ES
dc.description.monthDices_ES
dc.description.abstractotrodioma1. Intracellular Cl- activity (aiCl) and membrane potential (Em) were measured in frog dorsal root ganglion neurones (DRG neurones) using double-barrelled Cl- -selective microelectrodes. In standard Ringer solution buffered with HEPES (5 mM), equilibrated with air or 100% O2, the resting membrane potential was -57.7 +-- 1.0 mV and aiCl was 23.6 +-- 1.0 mM (n = 53). The value of aiCl was 2.6 times the activity expected for an equilibrium distribution and the difference between Em and ECl was 25 mV. 2. Removal of external Cl- led to a reversible fall in aiCl. Initial rates of decay and recovery of aiCl were 4.1 and 3.3 mM min-1, respectively. During the recovery of aiCl following return to standard Ringer solution, most of the movement of Cl- occurred against the driving force for a passive distribution. Changes in aiCl were not associated with changes in Em. Chloride fluxes estimated from initial rates of change in aiCl when external Cl- was removed were too high to be accounted for by electrodiffusion. 3. The intracellular accumulation of Cl- was dependent on the extracellular Cl- activity (aoCl). The relationship between aiCl and aoCl had a sigmoidal shape with a half-maximal activation of about 50 mM-external Cl-. 4. The steady-state aiCl depended on the simultaneous presence of extracellular Na+ and K+. Similarly, the active reaccumulation of Cl- after intracellular Cl- depletion was abolished in the absence of either Na+ or K+ in the bathing solution. 5. The reaccumulation of Cl- was inhibited by furosemide (0.5-1 x 10(-3) M) or bumetanide (10(-5) M). The decrease in aiCl observed in Cl- -free solutions was also inhibited by bumetanide. 6. Cell volume changes were calculated from the observed changes in aiCl. Cells were estimated to shrink in Cl- -free solutions to about 75% their initial volume, at an initial rate of 6% min-1. 7. The present results provide direct evidence for the active accumulation of Cl- in DRG neurones. The mechanism of Cl- transport is electrically silent, dependent on the simultaneous presence of external Cl-, Na+ and K+ and inhibited by loop diuretics. It is suggested that a Na+:K+:Cl- co-transport system mediates the active transport of Cl- across the cell membrane of DRG neurones.es_ES
dc.subject.koAction Potentialses_ES
dc.subject.koDrug Effectses_ES
dc.subject.koAnimalses_ES
dc.subject.koBiological Transport, Activees_ES
dc.subject.koChlorideses_ES
dc.subject.koPharmacologyes_ES
dc.subject.koPhysiologyes_ES
dc.subject.koDiureticses_ES
dc.subject.koGanglia, Spinales_ES
dc.subject.koMembrane Potentialses_ES
dc.subject.koNeuronses_ES
dc.subject.koPotassiumes_ES
dc.subject.koRanidaees_ES
dc.subject.koSodiumes_ES
dc.subject.koSulfonamideses_ES
dc.subject.koTime Factorses_ES


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