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dc.creatorDe Gortari, P.
dc.creatorRomero, F.
dc.creatorCisneros, M.
dc.creatorJoseph-Bravo, P.
dc.date.accessioned2017-06-29T04:36:43Z
dc.date.available2017-06-29T04:36:43Z
dc.date.issued2005es_ES
dc.identifier468es_ES
dc.identifier.issn0197-0186es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/5157
dc.identifier.urihttps://doi.org/10.1016/j.neuint.2004.11.002es_ES
dc.language.isoenges_ES
dc.relation46 (4) 347-356 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleAcute administration of alcohol modulates pyroglutamyl amino peptidase II activity and mRNA levels in rat limbic regionses_ES
dc.typearticlees_ES
dc.contributor.affiliationDepartment Neurociencias, Instituto Nacional de Psiquiatría, Ramón de la Fuente Muñiz, Calzada México-Xochimilco 101, Col. San Lorenzo Huipulco, C.P. 14370, Mexico.es_ES
dc.contributor.emailgortari@imp.edu.mxes_ES
dc.relation.jnabreviadoNEUROCHEM INTes_ES
dc.relation.journalNeurochemistry Internationales_ES
dc.identifier.placeInglaterraes_ES
dc.date.published2005es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1872-9754es_ES
dc.identifier.doi10.1016/j.neuint.2004.11.002es_ES
dc.description.monthMares_ES
dc.description.abstractotrodiomaReleased TRH is inactivated by an ectopeptidase, pyroglutamyl aminopeptidase II (PPII). PPII expression and activity are stringently regulated in adenohypophysis, and in rat brain, during kindling stimulation that activates TRHergic neurons. To gain further insight into the possible regulation of PPII, we studied the effect of an acute intraperitoneal ethanol administration that affects TRH content and expression. PPII activity was determined by a fluorometric assay and PPII mRNA levels by semi-quantitative RT-PCR. Activity decreased in frontal cortex 1 h after ethanol injection and, after 6 h, in hippocampus, amygdala and n. accumbens. PPII mRNA levels decreased at 30 and 60 min in frontal cortex and n. accumbens while increased at longer times in these regions and, in hippocampus and hypothalamus. NMDA and GABAA receptors’ agonists and antagonists were tested at 1 h (±ethanol) on PPII activity and mRNA levels, as well as on TRH content and its mRNA. In n. accumbens, PPII mRNA levels decreased by ethanol, MK-801, and muscimol while picrotoxin or NMDA reversed ethanol's inhibition. Ethanol decreased TRH content and increased TRH mRNA levels as MK-801 or muscimol did (NMDA or picrotoxin reverted the effect of ethanol). In frontal cortex, PPII activity was inhibited by ethanol, NMDA and MK-801 with ethanol; its mRNA levels were reduced by ethanol, MK-801 and muscimol (NMDA and picrotoxin reverted ethanol's inhibition). These results show that PPII expression and activity can be regulated in conditions where TRHergic neurons are modulated. Effects of ethanol on PPII mRNA levels as well as those of TRH and its mRNA may involve GABA or NMDA receptors in n. accumbens. Changes observed in frontal cortex suggest combined effects with stress. The response was region-specific in magnitude, tendency and kinetics. These results give further support for brain PPII regulation in conditions that modulate the activity of TRHergic neuronses_ES
dc.subject.koAlcohol-Induced Disorders, Nervous Systemes_ES
dc.subject.koenzymologyes_ES
dc.subject.koAlcohol-Induced Disorders, Nervous Systemes_ES
dc.subject.kogeneticses_ES
dc.subject.koAlcohol-Induced Disorders, Nervous Systemes_ES
dc.subject.kophysiopathologyes_ES
dc.subject.koAminopeptidaseses_ES
dc.subject.kodrug effectses_ES
dc.subject.koAminopeptidaseses_ES
dc.subject.kogeneticses_ES
dc.subject.kometabolismes_ES
dc.subject.koAnimalses_ES
dc.subject.koBrain Chemistryes_ES
dc.subject.kodrug effectses_ES
dc.subject.koBrain Chemistryes_ES
dc.subject.kogeneticses_ES
dc.subject.koDown-Regulationes_ES
dc.subject.kodrug effectses_ES
dc.subject.koDown-Regulationes_ES
dc.subject.kogeneticses_ES
dc.subject.koDrug Administration Schedulees_ES
dc.subject.koEthanoles_ES
dc.subject.kopharmacologyes_ES
dc.subject.koExcitatory Amino Acid Antagonistses_ES
dc.subject.kopharmacologyes_ES
dc.subject.koGABA Antagonistses_ES
dc.subject.kopharmacologyes_ES
dc.subject.koGABA-A Receptor Antagonistses_ES
dc.subject.koLimbic Systemes_ES
dc.subject.kodrug effectses_ES
dc.subject.koLimbic Systemes_ES
dc.subject.koenzymologyes_ES
dc.subject.koLimbic Systemes_ES
dc.subject.kophysiopathologyes_ES
dc.subject.koMalees_ES
dc.subject.koNeural Pathwayses_ES
dc.subject.kodrug effectses_ES
dc.subject.koNeural Pathwayses_ES
dc.subject.koenzymologyes_ES
dc.subject.koNeural Pathwayses_ES
dc.subject.kophysiopathologyes_ES
dc.subject.koNeuronses_ES
dc.subject.kodrug effectses_ES
dc.subject.koNeuronses_ES
dc.subject.koenzymologyes_ES
dc.subject.koPyrrolidonecarboxylic Acides_ES
dc.subject.koanalogs & derivativeses_ES
dc.subject.koPyrrolidonecarboxylic Acides_ES
dc.subject.kometabolismes_ES
dc.subject.koRNA, Messengeres_ES
dc.subject.kodrug effectses_ES
dc.subject.koRNA, Messengeres_ES
dc.subject.kometabolismes_ES
dc.subject.koRatses_ES
dc.subject.koRats, Wistares_ES
dc.subject.koReceptors, GABA-Aes_ES
dc.subject.kometabolismes_ES
dc.subject.koReceptors, N-Methyl-D-Aspartatees_ES
dc.subject.koantagonists & inhibitorses_ES
dc.subject.koReceptors, N-Methyl-D-Aspartatees_ES
dc.subject.kometabolismes_ES
dc.subject.koStress, Physiologicales_ES
dc.subject.kometabolismes_ES
dc.subject.koStress, Physiologicales_ES
dc.subject.kophysiopathologyes_ES
dc.subject.koThyrotropin-Releasing Hormonees_ES
dc.subject.kogeneticses_ES
dc.subject.koThyrotropin-Releasing Hormonees_ES
dc.subject.kometabolismes_ES
dc.subject.koExcitatory Amino Acid Antagonistses_ES
dc.subject.koGABA Antagonistses_ES
dc.subject.koGABA-A Receptor Antagonistses_ES
dc.subject.koRNA, Messengeres_ES
dc.subject.koReceptors, GABA-Aes_ES
dc.subject.koReceptors, N-Methyl-D-Aspartatees_ES
dc.subject.koThyrotropin-Releasing Hormonees_ES
dc.subject.koEthanoles_ES
dc.subject.koPyrrolidonecarboxylic Acides_ES
dc.subject.koAminopeptidaseses_ES
dc.subject.kopyroglutamyl-peptidase IIes_ES


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