Striatal Protection in nNOS Knock-Out Mice After Quinolinic Acid-Induced Oxidative Damage

Under pathological conditions, nitric oxide can become a mediator of oxidative cellular damage, generating an unbalance between oxidant and antioxidant systems. The participation of neuronal nitric oxide synthase (nNOS) in the neurodegeneration mechanism has been reported; the activation of N -methy...

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Bibliographic Details
Published in:Neurochemical research 2019-02, Vol.44 (2), p.421-427
Main Authors: Gerónimo-Olvera, C., Tristán-López, L., Martínez-Lazcano, J. C., García-Lara, L., Sánchez-Mendoza, A., Morales-Martínez, A., Hernández-Melesio, M. A., Arregui, L., Ríos, C., Pérez-Severiano, F.
Format: Article
Language:English
Subjects:
Antioxidants
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell Biology
Damage
Depletion
Excitotoxicity
Glutamic acid receptors (ionotropic)
Mice
N-Methyl-D-aspartic acid receptors
Neostriatum
Neurochemistry
Neurodegeneration
Neurology
Neurosciences
Nitric oxide
Nitric-oxide synthase
Occupational health
Original Paper
Oxidative stress
Quinolinic acid
Receptor mechanisms
Receptors
Saline solutions
Unbalance
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Summary:Under pathological conditions, nitric oxide can become a mediator of oxidative cellular damage, generating an unbalance between oxidant and antioxidant systems. The participation of neuronal nitric oxide synthase (nNOS) in the neurodegeneration mechanism has been reported; the activation of N -methyl- d -aspartate (NMDA) receptors by agonist quinolinic acid (QUIN) triggers an increase in nNOS function and promotes oxidative stress. The aim of the present work was to elucidate the participation of nNOS in QUIN-induced oxidative stress in knock-out mice (nNOS−/−). To do so, we microinjected saline solution or QUIN in the striatum of wild-type (nNOS +/+), heterozygote (nNOS+/−), and knock-out (nNOS−/−) mice, and measured circling behavior, GABA content levels, oxidative stress, and NOS expression and activity. We found that the absence of nNOS provides a protection against striatal oxidative damage induced by QUIN, resulting in decreased circling behavior, oxidative stress, and a partial protection reflected in GABA depletion. We have shown that nNOS-derived NO is involved in neurological damage induced by oxidative stress in a QUIN-excitotoxic model.
ISSN:0364-3190
1573-6903
DOI:10.1007/s11064-018-2688-3