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Early N-acetylaspartate depletion is a marker of neuronal dysfunction in rats and primates chronically treated with the mitochondrial toxin 3-nitropropionic acid.
J Cereb Blood Flow Metab. 2000 May; 20(5):789-99.JC

Abstract

N-acetylaspartate (NAA) quantification by 1H-magnetic resonance spectroscopy has been commonly used to assess in vivo neuronal loss in neurodegenerative disorders. Here. the authors used ex vivo and in vivo 1H-magnetic resonance spectroscopy in rat and primate models of progressive striatal degeneration induced by the mitochondrial toxin 3-nitropropionate (3NP) to determine whether early NAA depletions could also be associated with neuronal dysfunction. In rats that were treated for 3 days with 3NP and had motor symptoms, the authors found a significant decrease in NAA concentrations, specifically restricted to the striatum. No cell loss or dying cells were found at this stage in these animals. After 5 days of 3NP treatment, a further decrease in striatal NAA concentrations was observed in association with the occurrence of dying neurons in the dorsolateral striatum. In 3NP-treated primates, a similar striatal-selective and early decrease in NAA concentrations was observed after only a few weeks of neurotoxic treatment, without any sign of ongoing cell death. This early decrease in striatal NAA was partially reversed after 4 weeks of 3NP withdrawal. These results demonstrate that early NAA depletions reflect a reversible state of neuronal dysfunction preceding cell degeneration and suggest that in vivo quantification of NAA 1H-magnetic resonance spectroscopy may become a valuable tool for assessing early neuronal dysfunction and the effects of potential neuroprotective therapies in neurodegenerative disorders.

Authors+Show Affiliations

URA CEA CNRS 2210, Service Hospitalier Frédéric Joliot, Orsay, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10826529

Citation

Dautry, C, et al. "Early N-acetylaspartate Depletion Is a Marker of Neuronal Dysfunction in Rats and Primates Chronically Treated With the Mitochondrial Toxin 3-nitropropionic Acid." Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, vol. 20, no. 5, 2000, pp. 789-99.
Dautry C, Vaufrey F, Brouillet E, et al. Early N-acetylaspartate depletion is a marker of neuronal dysfunction in rats and primates chronically treated with the mitochondrial toxin 3-nitropropionic acid. J Cereb Blood Flow Metab. 2000;20(5):789-99.
Dautry, C., Vaufrey, F., Brouillet, E., Bizat, N., Henry, P. G., Condé, F., Bloch, G., & Hantraye, P. (2000). Early N-acetylaspartate depletion is a marker of neuronal dysfunction in rats and primates chronically treated with the mitochondrial toxin 3-nitropropionic acid. Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, 20(5), 789-99.
Dautry C, et al. Early N-acetylaspartate Depletion Is a Marker of Neuronal Dysfunction in Rats and Primates Chronically Treated With the Mitochondrial Toxin 3-nitropropionic Acid. J Cereb Blood Flow Metab. 2000;20(5):789-99. PubMed PMID: 10826529.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Early N-acetylaspartate depletion is a marker of neuronal dysfunction in rats and primates chronically treated with the mitochondrial toxin 3-nitropropionic acid. AU - Dautry,C, AU - Vaufrey,F, AU - Brouillet,E, AU - Bizat,N, AU - Henry,P G, AU - Condé,F, AU - Bloch,G, AU - Hantraye,P, PY - 2000/5/29/pubmed PY - 2000/6/10/medline PY - 2000/5/29/entrez SP - 789 EP - 99 JF - Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism JO - J Cereb Blood Flow Metab VL - 20 IS - 5 N2 - N-acetylaspartate (NAA) quantification by 1H-magnetic resonance spectroscopy has been commonly used to assess in vivo neuronal loss in neurodegenerative disorders. Here. the authors used ex vivo and in vivo 1H-magnetic resonance spectroscopy in rat and primate models of progressive striatal degeneration induced by the mitochondrial toxin 3-nitropropionate (3NP) to determine whether early NAA depletions could also be associated with neuronal dysfunction. In rats that were treated for 3 days with 3NP and had motor symptoms, the authors found a significant decrease in NAA concentrations, specifically restricted to the striatum. No cell loss or dying cells were found at this stage in these animals. After 5 days of 3NP treatment, a further decrease in striatal NAA concentrations was observed in association with the occurrence of dying neurons in the dorsolateral striatum. In 3NP-treated primates, a similar striatal-selective and early decrease in NAA concentrations was observed after only a few weeks of neurotoxic treatment, without any sign of ongoing cell death. This early decrease in striatal NAA was partially reversed after 4 weeks of 3NP withdrawal. These results demonstrate that early NAA depletions reflect a reversible state of neuronal dysfunction preceding cell degeneration and suggest that in vivo quantification of NAA 1H-magnetic resonance spectroscopy may become a valuable tool for assessing early neuronal dysfunction and the effects of potential neuroprotective therapies in neurodegenerative disorders. SN - 0271-678X UR - https://www.unboundmedicine.com/medline/citation/10826529/Early_N_acetylaspartate_depletion_is_a_marker_of_neuronal_dysfunction_in_rats_and_primates_chronically_treated_with_the_mitochondrial_toxin_3_nitropropionic_acid_ L2 - https://journals.sagepub.com/doi/10.1097/00004647-200005000-00005?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -