Mostrar el registro sencillo del ítem
Effects of chronic morphine and N(6)-cyclopentyl-adenosine administration on kainic acid-induced status epilepticus.
dc.creator | Cano-Martínez, Agustina | |
dc.creator | Villalobos-Molina, Rafael | |
dc.creator | Rocha, Luisa | |
dc.date.accessioned | 2017-06-30T03:55:08Z | |
dc.date.available | 2017-06-30T03:55:08Z | |
dc.date.issued | 2001 | es_ES |
dc.identifier | 2376 | es_ES |
dc.identifier.issn | 0920-1211 | es_ES |
dc.identifier.uri | http://repositorio.inprf.gob.mx/handle/123456789/7019 | |
dc.identifier.uri | https://doi.org/10.1016/S0920-1211(01)00187-5 | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Amsterdam : Elsevier Science Publishers | es_ES |
dc.relation | 44 (2-3) 89-96 p. | es_ES |
dc.relation | versión del editor | es_ES |
dc.rights | acceso cerrado | es_ES |
dc.subject.mesh | Adenosine-Analogs & derivatives | es_ES |
dc.subject.mesh | Adenosine-Pharmacology | es_ES |
dc.subject.mesh | Analgesics, Opioid - Pharmacology | es_ES |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Behavior, Animal- Drug effects | es_ES |
dc.subject.mesh | Behavior, Animal-Physiology | es_ES |
dc.subject.mesh | Excitatory Amino Acid Agonists | es_ES |
dc.subject.mesh | Kainic Acid | es_ES |
dc.subject.mesh | Male | es_ES |
dc.subject.mesh | Morphine-Pharmacology | es_ES |
dc.subject.mesh | Rats | es_ES |
dc.subject.mesh | Rats, Wistar | es_ES |
dc.subject.mesh | Receptors, Opioid, mu - Drug effects | es_ES |
dc.subject.mesh | Receptors, Opioid, mu - Metabolism | es_ES |
dc.subject.mesh | Receptors, Purinergic P1 - Drug effects | es_ES |
dc.subject.mesh | Receptors, Purinergic P1 - Metabolism | es_ES |
dc.subject.mesh | Status Epilepticus-Chemically induced | es_ES |
dc.subject.mesh | Status Epilepticus-Metabolism | es_ES |
dc.subject.mesh | Up-Regulation-Drug effects | es_ES |
dc.subject.mesh | Up-Regulation-Physiology | es_ES |
dc.subject.mesh | Analgesics, Opioid | es_ES |
dc.subject.mesh | Excitatory Amino Acid Agonists | es_ES |
dc.subject.mesh | Receptors, Opioid, mu | es_ES |
dc.subject.mesh | Receptors, Purinergic P1 | es_ES |
dc.subject.mesh | N(6)-cyclopentyladenosine | es_ES |
dc.subject.mesh | Morphine | es_ES |
dc.subject.mesh | Adenosine | es_ES |
dc.subject.mesh | Kainic Acid | es_ES |
dc.title | Effects of chronic morphine and N(6)-cyclopentyl-adenosine administration on kainic acid-induced status epilepticus. | es_ES |
dc.type | article | es_ES |
dc.contributor.affiliation | Departamento de Fisiología, Instituto Nacional de Cardiología "Ignacio Chávez", Juan Badiano #1 CP 14080, Mexico , D.F | es_ES |
dc.relation.jnabreviado | EPILEPSY RES | es_ES |
dc.relation.journal | Epilepsy Research | es_ES |
dc.identifier.place | Países Bajos | es_ES |
dc.date.published | 2001 | es_ES |
dc.identifier.organizacion | Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz | es_ES |
dc.identifier.doi | 10.1016/S0920-1211(01)00187-5 | es_ES |
dc.description.month | May | es_ES |
dc.description.abstractotrodioma | The 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 |
Ficheros en el ítem
Ficheros | Tamaño | Formato | Ver |
---|---|---|---|
No hay ficheros asociados a este ítem. |