Ascorbate neurotoxicity in cortical cell culture

Kinya Hisanaga, Stephen M. Sagar, Frank R Sharp

Research output: Contribution to journalArticle

29 Citations (Scopus)

Abstract

Ascorbate (vitamin C) is believed to act as a neuromodulator that facilitates the release of neurotransmitters and inhibits neurotransmitter binding to receptors, including dopamine and N-methyl-D-aspartate receptors. Extracellular levels of ascorbate are known to reach the low millimolar range after ischemic brain injury. This study shows that treatment of cultured cortical neurons with micromolar to low millimolar ascorbate first inhibits total protein synthesis and then results in late neuronal death. Astrocytes are much less vulnerable to ascorbate than neurons. Ascorbate may exacerbate neuronal and glial damage after brain ischemia, and it may play a pathological role in other neurological diseases.

Original languageEnglish (US)
Pages (from-to)562-565
Number of pages4
JournalAnnals of Neurology
Volume31
Issue number5
StatePublished - May 1992
Externally publishedYes

Fingerprint

Neurotransmitter Agents
Cell Culture Techniques
Neurons
Dopamine Receptors
N-Methyl-D-Aspartate Receptors
Brain Ischemia
Neuroglia
Astrocytes
Brain Injuries
Ascorbic Acid
Proteins

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Ascorbate neurotoxicity in cortical cell culture. / Hisanaga, Kinya; Sagar, Stephen M.; Sharp, Frank R.

In: Annals of Neurology, Vol. 31, No. 5, 05.1992, p. 562-565.

Research output: Contribution to journalArticle

Hisanaga, K, Sagar, SM & Sharp, FR 1992, 'Ascorbate neurotoxicity in cortical cell culture', Annals of Neurology, vol. 31, no. 5, pp. 562-565.
Hisanaga, Kinya ; Sagar, Stephen M. ; Sharp, Frank R. / Ascorbate neurotoxicity in cortical cell culture. In: Annals of Neurology. 1992 ; Vol. 31, No. 5. pp. 562-565.
@article{0b99df8e2d7a46b98a6cd0cea9748f34,
title = "Ascorbate neurotoxicity in cortical cell culture",
abstract = "Ascorbate (vitamin C) is believed to act as a neuromodulator that facilitates the release of neurotransmitters and inhibits neurotransmitter binding to receptors, including dopamine and N-methyl-D-aspartate receptors. Extracellular levels of ascorbate are known to reach the low millimolar range after ischemic brain injury. This study shows that treatment of cultured cortical neurons with micromolar to low millimolar ascorbate first inhibits total protein synthesis and then results in late neuronal death. Astrocytes are much less vulnerable to ascorbate than neurons. Ascorbate may exacerbate neuronal and glial damage after brain ischemia, and it may play a pathological role in other neurological diseases.",
author = "Kinya Hisanaga and Sagar, {Stephen M.} and Sharp, {Frank R}",
year = "1992",
month = "5",
language = "English (US)",
volume = "31",
pages = "562--565",
journal = "Annals of Neurology",
issn = "0364-5134",
publisher = "John Wiley and Sons Inc.",
number = "5",

}

TY - JOUR

T1 - Ascorbate neurotoxicity in cortical cell culture

AU - Hisanaga, Kinya

AU - Sagar, Stephen M.

AU - Sharp, Frank R

PY - 1992/5

Y1 - 1992/5

N2 - Ascorbate (vitamin C) is believed to act as a neuromodulator that facilitates the release of neurotransmitters and inhibits neurotransmitter binding to receptors, including dopamine and N-methyl-D-aspartate receptors. Extracellular levels of ascorbate are known to reach the low millimolar range after ischemic brain injury. This study shows that treatment of cultured cortical neurons with micromolar to low millimolar ascorbate first inhibits total protein synthesis and then results in late neuronal death. Astrocytes are much less vulnerable to ascorbate than neurons. Ascorbate may exacerbate neuronal and glial damage after brain ischemia, and it may play a pathological role in other neurological diseases.

AB - Ascorbate (vitamin C) is believed to act as a neuromodulator that facilitates the release of neurotransmitters and inhibits neurotransmitter binding to receptors, including dopamine and N-methyl-D-aspartate receptors. Extracellular levels of ascorbate are known to reach the low millimolar range after ischemic brain injury. This study shows that treatment of cultured cortical neurons with micromolar to low millimolar ascorbate first inhibits total protein synthesis and then results in late neuronal death. Astrocytes are much less vulnerable to ascorbate than neurons. Ascorbate may exacerbate neuronal and glial damage after brain ischemia, and it may play a pathological role in other neurological diseases.

UR - http://www.scopus.com/inward/record.url?scp=0026510034&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026510034&partnerID=8YFLogxK

M3 - Article

C2 - 1596092

AN - SCOPUS:0026510034

VL - 31

SP - 562

EP - 565

JO - Annals of Neurology

JF - Annals of Neurology

SN - 0364-5134

IS - 5

ER -