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Sodium bromide: effects on different patterns of epileptiform activity, extracellular pH changes and GABAergic inhibition

dc.creatorMeierkord, H.
dc.creatorGrunig, F.
dc.creatorGutschmidt, U.
dc.creatorGutiérrez, R.
dc.creatorPfeiffer, M.
dc.creatorDraguhn, A.
dc.creatorBruckner, C.
dc.creatorHeinemann, U.
dc.date.accessioned2017-06-30T04:03:30Z
dc.date.available2017-06-30T04:03:30Z
dc.date.issued2000es_ES
dc.identifier2478es_ES
dc.identifier.issn0028-1298es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/7119
dc.identifier.urihttps://doi.org/10.1007/s002109900162es_ES
dc.language.isoenges_ES
dc.publisherSPRINGER VERLAG, 175 FIFTH AVE, NEW YORK, NY 10010 USAes_ES
dc.relation361 (1) 25-32 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleSodium bromide: effects on different patterns of epileptiform activity, extracellular pH changes and GABAergic inhibitiones_ES
dc.typearticlees_ES
dc.contributor.affiliationHumboldt Univ, Neurol Klin & Poliklin, Klinikum Charite, Schumannstr 20-21, D-10117 Berlin, Germanyes_ES
dc.relation.jnabreviadoNAUNYN SCHMIEDEBERGS ARCH PHARMACOLes_ES
dc.relation.journalNaunyn-Schmiedeberg's archives of pharmacologyes_ES
dc.identifier.placeNew Yorkes_ES
dc.date.published2000es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, México.es_ES
dc.identifier.eissn1432-1912es_ES
dc.identifier.doi10.1007/s002109900162es_ES
dc.description.monthEnees_ES
dc.description.abstractotrodiomaResults regarding the anticonvulsant potency of bromide have been questioned, and the mechanisms of its action are unclear. Using combined rat hippocampus entorhinal cortex slices we analyzed the effects of NaBr on four types of epileptiform discharges in two different models of epilepsy, the low-Ca2+ and the low-Mg2+ model. NaBr concentration-dependently reduced the frequency and finally blocked the low Ca2+-induced discharges. Low Mg2+-induced short recurrent discharges were also reduced in a concentration-dependent manner. In the entorhinal cortex the frequency of seizure-like events was reduced by 3 and 5 mM and the discharges were blocked by 7 mM NaBr. Also, the late recurrent discharges in the entorhinal cortex which do not respond to most clinically employed anticonvulsants were reduced by concentrations of 10 and 15 mM and completely blocked by 30 mM NaBr. Using pH-sensitive microelectrodes different effects of NaBr were seen than those of acetazolamide on extracellular pH under control conditions and after stimulation. Acetazolamide at 1 mM caused a reversible acidification of Delta pH: 0.2+/-0.14 at rest whereas no change on extracellular pH was seen with 5 mM NaBr. Acetazolamide increased the transient alkalosis induced by repetitive stimulation of the stratum radiatum in area CAI and reduced the subsequent acidosis. NaBr also increased the alkalosis but had no effect on the subsequent acidosis. A significant increase in paired-pulse inhibition was seen in a paired-pulse stimulation protocol used to monitor the efficacy of GABAergic inhibition at concentrations of 5 mM NaBr. This finding was confirmed in whole-cell patch clamp recordings from cultured hippocampal neurons showing an increase in inhibitory postsynaptic current amplitude. In summary, our results suggest a broad-spectrum anticonvulsant activity which is likely to be caused by its effects on membrane excitability, by an increase in GABAergic inhibition and is less likely caused by its effects on extracellular pH.es_ES


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