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Year 2019, , 5 - 5, 21.06.2019
https://doi.org/10.37212/jcnos.584662

Abstract

References

  • Choi DW. 1992. Excitotoxic cell death. J. Neurobiol. 23:1261–1276.
  • Olney JW. 1969. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science (80-. ). 164:719–721.
  • Koh JY, Choi DW. 1988. Vulnerability of cultured cortical neurons to damage by excitotoxins: differential susceptibility of neurons containing NADPH-diaphorase. J. Neurosci. 8:2153–2163.

Intracellular zinc mobilization is required for nNOS (+) neuron loss. Role of zinc in the excitotoxic cascade

Year 2019, , 5 - 5, 21.06.2019
https://doi.org/10.37212/jcnos.584662

Abstract

NMDA receptor (NMDAR) overstimulation by glutamate promotes massive calcium (Ca2+) entry and initiates a cascade of events leading to the overproduction of Reactive Oxygen Species (ROS), mitochondrial dysfunction, intraneuronal zinc (Zn2+) mobilization, and, ultimately, neuronal demise (Choi 1992).  This glutamate-driven form of neuronal death has been described as excitotoxicity (Olney 1969).  NADPH-diaphorase neurons [nNOS (+) neurons] are a subpopulation of nitric-oxide synthase-overexpressing interneurons that is spared from the NMDAR-mediated neuronal death (Koh and Choi, 1988).  The mechanisms underlying the reduced vulnerability of nNOS (+) neurons to NMDAR-driven neuronal death are still largely unexplored.  In the talk, we will discuss the mechanisms that are involved in the reduced vulnerability of nNOS (+) neurons.  Differences between nNOS (+) and nNOS (-) neurons as far as changes in intracellular Ca2+ levels, mitochondrial functioning, ROS production as well as the intraneuronal accumulation of Zn2+ were investigated.  We found that nNOS (+) neurons differ from nNOS (-) cells by lacking the production of a significant amount of ROS in response to NMDAR activation.  The absence of NMDA-driven oxidative stress shown by the nNOS (+) neurons abolished the neurotoxic accumulation of Zn2+.  Exposure of nNOS (-) neurons to NMDA in the presence of TPEN (a Zn2+ chelator) mimicked the behavior of the nNOS (+) subpopulation and preserved the nNOS (-) population from the excitotoxic damage.  These results indicate that Zn2+ mobilization is the mandatory step of the excitotoxic cascade.  These findings identify the intraneuronal accumulation of Zn2+ as a therapeutic target for the treatment of excitotoxic prone neurological conditions. 

References

  • Choi DW. 1992. Excitotoxic cell death. J. Neurobiol. 23:1261–1276.
  • Olney JW. 1969. Brain lesions, obesity, and other disturbances in mice treated with monosodium glutamate. Science (80-. ). 164:719–721.
  • Koh JY, Choi DW. 1988. Vulnerability of cultured cortical neurons to damage by excitotoxins: differential susceptibility of neurons containing NADPH-diaphorase. J. Neurosci. 8:2153–2163.
There are 3 citations in total.

Details

Primary Language English
Subjects Medical Physiology
Journal Section Original Articles
Authors

Alberto Granzotto This is me

Publication Date June 21, 2019
Published in Issue Year 2019

Cite

APA Granzotto, A. (2019). Intracellular zinc mobilization is required for nNOS (+) neuron loss. Role of zinc in the excitotoxic cascade. Journal of Cellular Neuroscience and Oxidative Stress, 11, 5-5. https://doi.org/10.37212/jcnos.584662
AMA Granzotto A. Intracellular zinc mobilization is required for nNOS (+) neuron loss. Role of zinc in the excitotoxic cascade. J Cell Neurosci Oxid Stress. June 2019;11:5-5. doi:10.37212/jcnos.584662
Chicago Granzotto, Alberto. “Intracellular Zinc Mobilization Is Required for NNOS (+) Neuron Loss. Role of Zinc in the Excitotoxic Cascade”. Journal of Cellular Neuroscience and Oxidative Stress 11, June (June 2019): 5-5. https://doi.org/10.37212/jcnos.584662.
EndNote Granzotto A (June 1, 2019) Intracellular zinc mobilization is required for nNOS (+) neuron loss. Role of zinc in the excitotoxic cascade. Journal of Cellular Neuroscience and Oxidative Stress 11 5–5.
IEEE A. Granzotto, “Intracellular zinc mobilization is required for nNOS (+) neuron loss. Role of zinc in the excitotoxic cascade”, J Cell Neurosci Oxid Stress, vol. 11, pp. 5–5, 2019, doi: 10.37212/jcnos.584662.
ISNAD Granzotto, Alberto. “Intracellular Zinc Mobilization Is Required for NNOS (+) Neuron Loss. Role of Zinc in the Excitotoxic Cascade”. Journal of Cellular Neuroscience and Oxidative Stress 11 (June 2019), 5-5. https://doi.org/10.37212/jcnos.584662.
JAMA Granzotto A. Intracellular zinc mobilization is required for nNOS (+) neuron loss. Role of zinc in the excitotoxic cascade. J Cell Neurosci Oxid Stress. 2019;11:5–5.
MLA Granzotto, Alberto. “Intracellular Zinc Mobilization Is Required for NNOS (+) Neuron Loss. Role of Zinc in the Excitotoxic Cascade”. Journal of Cellular Neuroscience and Oxidative Stress, vol. 11, 2019, pp. 5-5, doi:10.37212/jcnos.584662.
Vancouver Granzotto A. Intracellular zinc mobilization is required for nNOS (+) neuron loss. Role of zinc in the excitotoxic cascade. J Cell Neurosci Oxid Stress. 2019;11:5-.