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dc.creatorCano-Martínez, Agustina
dc.creatorVillalobos-Molina, Rafael
dc.creatorRocha, Luisa
dc.date.accessioned2017-06-30T03:55:08Z
dc.date.available2017-06-30T03:55:08Z
dc.date.issued2001es_ES
dc.identifier2376es_ES
dc.identifier.issn0920-1211es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/7019
dc.identifier.urihttps://doi.org/10.1016/S0920-1211(01)00187-5es_ES
dc.language.isoenges_ES
dc.publisherAmsterdam : Elsevier Science Publisherses_ES
dc.relation44 (2-3) 89-96 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.subject.meshAdenosine-Analogs & derivativeses_ES
dc.subject.meshAdenosine-Pharmacologyes_ES
dc.subject.meshAnalgesics, Opioid - Pharmacologyes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshBehavior, Animal- Drug effectses_ES
dc.subject.meshBehavior, Animal-Physiologyes_ES
dc.subject.meshExcitatory Amino Acid Agonistses_ES
dc.subject.meshKainic Acides_ES
dc.subject.meshMalees_ES
dc.subject.meshMorphine-Pharmacologyes_ES
dc.subject.meshRatses_ES
dc.subject.meshRats, Wistares_ES
dc.subject.meshReceptors, Opioid, mu - Drug effectses_ES
dc.subject.meshReceptors, Opioid, mu - Metabolismes_ES
dc.subject.meshReceptors, Purinergic P1 - Drug effectses_ES
dc.subject.meshReceptors, Purinergic P1 - Metabolismes_ES
dc.subject.meshStatus Epilepticus-Chemically inducedes_ES
dc.subject.meshStatus Epilepticus-Metabolismes_ES
dc.subject.meshUp-Regulation-Drug effectses_ES
dc.subject.meshUp-Regulation-Physiologyes_ES
dc.subject.meshAnalgesics, Opioides_ES
dc.subject.meshExcitatory Amino Acid Agonistses_ES
dc.subject.meshReceptors, Opioid, mues_ES
dc.subject.meshReceptors, Purinergic P1es_ES
dc.subject.meshN(6)-cyclopentyladenosinees_ES
dc.subject.meshMorphinees_ES
dc.subject.meshAdenosinees_ES
dc.subject.meshKainic Acides_ES
dc.titleEffects of chronic morphine and N(6)-cyclopentyl-adenosine administration on kainic acid-induced status epilepticus.es_ES
dc.typearticlees_ES
dc.contributor.affiliationDepartamento de Fisiología, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano #1 CP 14080, Mexico , D.Fes_ES
dc.relation.jnabreviadoEPILEPSY RESes_ES
dc.relation.journalEpilepsy Researches_ES
dc.identifier.placePaíses Bajoses_ES
dc.date.published2001es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.doi10.1016/S0920-1211(01)00187-5es_ES
dc.description.monthMayes_ES
dc.description.abstractotrodiomaThe aim of the present study was to investigate if the upregulation of mu or A(1) receptors modifies the expression of the kainic acid (KA)-induced status epilepticus (SE). Male Wistar rats received one of the following treatments: saline solution (SS) (1 ml/kg, i.p. for 7 days)| morphine (M) (20 mg/kg, i.p. for 7 days) or N(6)-cyclopentyl-adenosine (CPA) (1 mg/kg, i.p. for 9 days). Twenty-four hours after the last administration rats were sacrificed. Membranes were obtained mu and and A(1) receptor binding experiments were carried out. Furthermore, an injection of SS (1 ml/kg, i.p.) or KA (10 mg/kg, i.p.) was applied in rats pretreated chronically with M, CPA or SS, 48 h after the last administration. Seizure activity, death rate and a postictal explosive motor behavior were evaluated after KA administration. Chronic M administration increased mu receptor number in hippocampus (115%) and cortex (265%), whereas chronic CPA treatment enhanced A(1) receptor number in hippocampus (55%), amygdala (39%) and cortex (51%). The pretreatment with M facilitated the KA-induced SE and reduced the death rate as well as the postictal explosive motor behavior. The pretreatment with CPA delayed the SE presentation, increased the death rate and decreased the postictal explosive motor behavior. These findings suggest that upregulation of mu receptors enhances the KA seizures, whereas upregulation of A(1) receptors depresses these seizures.es_ES


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