Neurochemical Research

, Volume 44, Issue 2, pp 421–427 | Cite as

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

  • C. Gerónimo-Olvera
  • L. Tristán-López
  • J. C. Martínez-Lazcano
  • L. García-Lara
  • A. Sánchez-Mendoza
  • A. Morales-Martínez
  • M. A. Hernández-Melesio
  • L. Arregui
  • C. Ríos
  • F. Pérez-SeverianoEmail author
Original Paper


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.


Excitotoxicity Quinolinic acid Nitric oxide synthase Oxidative stress Neuronal nitric oxide synthase knock-out mice 



Circling behavior




2’,7’-Dichlorodihydrofluorescein diacetate


Enhanced chemiluminescence


Huntington’s disease


High-performance liquid chromatography


Lipid peroxidation




Nitric oxide


Neuronal nitric oxide synthase


Optical density


Quinolinic acid


Reactive oxygen species


Standard error of the mean


Saline solution



This work was supported by Conacyt Grant CB-2014 #241911 to F.P-S and was partially supported by Grant FOSISS-2015-2-261721 to L.T-L.


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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  • C. Gerónimo-Olvera
    • 1
  • L. Tristán-López
    • 1
  • J. C. Martínez-Lazcano
    • 2
  • L. García-Lara
    • 1
  • A. Sánchez-Mendoza
    • 3
  • A. Morales-Martínez
    • 1
  • M. A. Hernández-Melesio
    • 1
  • L. Arregui
    • 4
  • C. Ríos
    • 1
  • F. Pérez-Severiano
    • 1
    Email author
  1. 1.Departamento de NeuroquímicaInstituto Nacional de Neurología y Neurocirugía Manuel Velasco SuárezCiudad de MéxicoMexico
  2. 2.Departamento de NeurofisiologíaInstituto Nacional de Neurología y Neurocirugía Manuel Velasco SuárezCiudad de MéxicoMéxico
  3. 3.Departamento de FarmacologíaInstituto Nacional de Cardiología Ignacio ChávezCiudad de MéxicoMexico
  4. 4.Departamento de Ciencias Naturales, División de Ciencias Naturales e IngenieríaUniversidad Autónoma Metropolitana-Unidad CuajimalpaCiudad de MéxicoMexico

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