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Time-related changes in constitutive and inducible nitric oxide synthases in the rat striatum in a model of Huntington's disease.
Neurotoxicology. 2007 Nov; 28(6):1200-7.N

Abstract

Excitotoxicity and oxidative stress are mechanisms involved in the neuronal cell death induced by the intrastriatal injection of quinolinic acid (QUIN) as a model of Huntington's disease. Production of nitric oxide by nitric oxide synthase (NOS) has been proposed to participate in QUIN-induced neurotoxicity; however, the precise role of NOS in QUIN-induced toxicity still remains controversial. In order to provide further information on the role of NOS isoforms in QUIN toxicity, we performed real time RT-PCR and immunohistochemistry of inducible NOS (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS) and determined Ca(2+)-dependent and Ca(2+)-independent NOS activity in a temporal course (3-48h), after an intrastriatal injection of QUIN to rats. NOS isoforms exhibited a transitory expression of mRNA and protein after QUIN infusion: eNOS increased between 3 and 24h, iNOS between 12 and 24h, while nNOS at 35 and 48h. Ca(2+)-independent activity (iNOS) did not show any change, while Ca(2+)-dependent activity (constitutive NOS: eNOS/nNOS) exhibited increased levels at 3h. Our results support the participation of Ca(2+)-dependent NOS isoforms during the toxic events produced at early times after QUIN injection.

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Authors+Show Affiliations

Aguilera P
Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía Manuel Velasco Suárez, México, DF 14269, Mexico.
Chánez-Cárdenas ME
No affiliation info available
Floriano-Sánchez E
No affiliation info available
Barrera D
No affiliation info available
Santamaría A
No affiliation info available
Sánchez-González DJ
No affiliation info available
Pérez-Severiano F
No affiliation info available
Pedraza-Chaverrí J
No affiliation info available
Jiménez PD
No affiliation info available

MeSH

AnimalsBasal GangliaCalciumDisease Models, AnimalGene Expression Regulation, EnzymologicHuntington DiseaseImmunohistochemistryMaleNitric OxideNitric Oxide SynthaseNitric Oxide Synthase Type INitric Oxide Synthase Type IINitric Oxide Synthase Type IIIQuinolinic AcidRNA, MessengerRatsRats, WistarReverse Transcriptase Polymerase Chain ReactionTime FactorsUp-Regulation

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17850874

Citation

Aguilera, Penélope, et al. "Time-related Changes in Constitutive and Inducible Nitric Oxide Synthases in the Rat Striatum in a Model of Huntington's Disease." Neurotoxicology, vol. 28, no. 6, 2007, pp. 1200-7.
Aguilera P, Chánez-Cárdenas ME, Floriano-Sánchez E, et al. Time-related changes in constitutive and inducible nitric oxide synthases in the rat striatum in a model of Huntington's disease. Neurotoxicology. 2007;28(6):1200-7.
Aguilera, P., Chánez-Cárdenas, M. E., Floriano-Sánchez, E., Barrera, D., Santamaría, A., Sánchez-González, D. J., Pérez-Severiano, F., Pedraza-Chaverrí, J., & Jiménez, P. D. (2007). Time-related changes in constitutive and inducible nitric oxide synthases in the rat striatum in a model of Huntington's disease. Neurotoxicology, 28(6), 1200-7.
Aguilera P, et al. Time-related Changes in Constitutive and Inducible Nitric Oxide Synthases in the Rat Striatum in a Model of Huntington's Disease. Neurotoxicology. 2007;28(6):1200-7. PubMed PMID: 17850874.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Time-related changes in constitutive and inducible nitric oxide synthases in the rat striatum in a model of Huntington's disease. AU - Aguilera,Penélope, AU - Chánez-Cárdenas,María Elena, AU - Floriano-Sánchez,Esaú, AU - Barrera,Diana, AU - Santamaría,Abel, AU - Sánchez-González,Dolores Javier, AU - Pérez-Severiano,Francisca, AU - Pedraza-Chaverrí,José, AU - Jiménez,Perla Deyanira Maldonado, Y1 - 2007/08/06/ PY - 2007/03/14/received PY - 2007/07/27/revised PY - 2007/07/30/accepted PY - 2007/9/14/pubmed PY - 2008/2/8/medline PY - 2007/9/14/entrez SP - 1200 EP - 7 JF - Neurotoxicology JO - Neurotoxicology VL - 28 IS - 6 N2 - Excitotoxicity and oxidative stress are mechanisms involved in the neuronal cell death induced by the intrastriatal injection of quinolinic acid (QUIN) as a model of Huntington's disease. Production of nitric oxide by nitric oxide synthase (NOS) has been proposed to participate in QUIN-induced neurotoxicity; however, the precise role of NOS in QUIN-induced toxicity still remains controversial. In order to provide further information on the role of NOS isoforms in QUIN toxicity, we performed real time RT-PCR and immunohistochemistry of inducible NOS (iNOS), endothelial NOS (eNOS) and neuronal NOS (nNOS) and determined Ca(2+)-dependent and Ca(2+)-independent NOS activity in a temporal course (3-48h), after an intrastriatal injection of QUIN to rats. NOS isoforms exhibited a transitory expression of mRNA and protein after QUIN infusion: eNOS increased between 3 and 24h, iNOS between 12 and 24h, while nNOS at 35 and 48h. Ca(2+)-independent activity (iNOS) did not show any change, while Ca(2+)-dependent activity (constitutive NOS: eNOS/nNOS) exhibited increased levels at 3h. Our results support the participation of Ca(2+)-dependent NOS isoforms during the toxic events produced at early times after QUIN injection. SN - 0161-813X UR - https://www.unboundmedicine.com/medline/citation/17850874/Time_related_changes_in_constitutive_and_inducible_nitric_oxide_synthases_in_the_rat_striatum_in_a_model_of_Huntington's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0161-813X(07)00164-7 DB - PRIME DP - Unbound Medicine ER -