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NAP protects against cyanide-related microtubule destruction

  • Basic Neurosciences, Genetics and Immunology - Review Article
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Abstract

The peptide NAP (NAPVSIPQ) was shown to protect neurons against a wide variety of insults. Particularly, NAP was shown to be neuroprotective in vitro against cyanide in hippocampal cultures and against oxygen-glucose deprivation in hippocampal and cortical neuronal cultures. Cyanide causes energy depletion in the cell and destroys the cytoskeleton, and NAP has been shown before to protect the microtubule cytoskeleton. The current study explored the effect of NAP on cyanide-induced microtubule destruction in cerebral cortical cultures. Sodium cyanide (6.8 mM) reduced the number of neurons containing intact microtubules as identified by bIII-tubulin immunostaining. When sodium cyanide was added together with NAP (10−14–10−12 M), complete protection was observed. Although the primary site of action of cyanide is considered to be the mitochondria, the current results involve microtubule destruction by cyanide toxicity that is completely reversed by NAP treatment.

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Acknowledgments

These studies are in partial fulfillment of the PhD requirements for Mrs. Ilona Zemlyak at the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Professor Illana Gozes is the incumbent of Lily and Avraham Gildor Chair for the Investigation of Growth Factors and serves as the Director of the Adams Super Center for Brain Studies, the Edersheim Levie-Gitter Institute for Functional Brain Imaging and the Dr. Diana and Zelman Elton (Elbaum) Laboratory for Molecular Neuroendocrinology. Professor Illana Gozes serves as the Chief Scientific Officer of Allon Therapeutics Inc. and the President of the Israel Society for Neuroscience. Professor Robert Sapolsky is the John A and Cynthia Fry Gunn Professor at Stanford University. Supported in part by the US-Israel Binational Science Foundation and by Allon Therapeutics Inc.

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Zemlyak, I., Sapolsky, R. & Gozes, I. NAP protects against cyanide-related microtubule destruction. J Neural Transm 116, 1411–1416 (2009). https://doi.org/10.1007/s00702-009-0252-7

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  • DOI: https://doi.org/10.1007/s00702-009-0252-7

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