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Titolo:
Attenuation of malonate toxicity in primary mesencephalic cultures using the GABA transport blocker, NO-711
Autore:
Stokes, AH; Bernard, LP; Nicklas, WJ; Zeevalk, GD;
Indirizzi:
Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Neurol, Piscataway, NJ 08854 USA Univ Med & Dent New Jersey Piscataway NJ USA 08854 scataway, NJ 08854 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE RESEARCH
fascicolo: 1, volume: 64, anno: 2001,
pagine: 43 - 52
SICI:
0360-4012(20010401)64:1<43:AOMTIP>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
NIGROSTRIATAL DOPAMINERGIC-NEURONS; EXCITOTOXIC CELL-DEATH; OXIDATIVE STRESS; SUCCINATE-DEHYDROGENASE; PARKINSONS-DISEASE; SELECTIVE VULNERABILITY; RECEPTOR ACTIVATION; INHIBITOR MALONATE; ENERGY-METABOLISM; KINDLING MODEL;
Keywords:
nipecotic acid; mitochondria; reactive oxygen species; energy impairment;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Zeevalk, GD Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Neurol, 675 Hoes Lane, Piscataway, NJ 08854 USA Univ Med & Dent New Jersey 675 Hoes Lane Piscataway NJ USA 08854
Citazione:
A.H. Stokes et al., "Attenuation of malonate toxicity in primary mesencephalic cultures using the GABA transport blocker, NO-711", J NEUROSC R, 64(1), 2001, pp. 43-52

Abstract

Cultured rat mesencephalic neurons were used to assess the effects of gamma -aminobutyric acid (GABA) transport blockers on toxicity caused by malonate, a reversible, competitive inhibitor of succinate dehydrogenase. Previous studies utilizing an ex vive chick retinal preparation have shown that GABA release and cell swelling are early consequences of acute energy impairment and that GABA transport blockers attenuate this toxicity. The present results demonstrate that the nonsubstrate GABA transport blocker, NO-711 (1 nM-1 muM), dose-dependently protected cultured mesencephalic dopamine (DA) and GABA neurons from malonate-induced toxicity. Similar protection was demonstrated with nipecotic acid (1 mM) and SKF89976A (100 nM), substrate and nonsubstrate GABA transport blockers, respectively. These compounds by themselves produced no signs of toxicity, although nipecotic acid caused a long-term decrease in GABA uptake not associated with toxicity. Compounds whichdecrease intracellular reactive oxygen species (ROS) are protective in this model, but NO-711 did not prevent the rise in intracellular ROS induced by malonate, indicating its protective effects were downstream of ROS production. Supplementation of malonate treated cultures with the GABA, agonist, muscimol (10 muM), increased the toxicity toward the DA and GABA neuron populations. Antagonists at the GABA, and glycine receptors provided partial protection to both the GABA and DA neurons. These findings suggest that the GABA transporter, GABA(A), and/or glycine channels contribute to cell damage associated with energy impairment in this model. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 15:02:08