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Titolo:
EXCITOTOXICITY IN THE ENTERIC NERVOUS-SYSTEM
Autore:
KIRCHGESSNER AL; LIU MT; ALCANTARA F;
Indirizzi:
COLUMBIA UNIV COLL PHYS & SURG,DEPT ANAT & CELL BIOL,630 W 168TH ST NEW YORK NY 10032
Titolo Testata:
The Journal of neuroscience
fascicolo: 22, volume: 17, anno: 1997,
pagine: 8804 - 8816
SICI:
0270-6474(1997)17:22<8804:EITEN>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTAMATE-RECEPTOR SUBUNITS; ASPARTATE NMDAR1 RECEPTOR; CORTICAL CELL-CULTURE; GUINEA-PIG ILEUM; IMMUNOCYTOCHEMICAL LOCALIZATION; MYENTERIC PLEXUS; NEURONAL DEATH; NITRIC-OXIDE; MESSENGER-RNA; CL SECRETION;
Keywords:
NECROSIS; APOPTOSIS; NMDA; KAINIC ACID; GLUTAMATE TRANSPORTERS; BLEB FORMATION; RHODAMINE 123;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
53
Recensione:
Indirizzi per estratti:
Citazione:
A.L. Kirchgessner et al., "EXCITOTOXICITY IN THE ENTERIC NERVOUS-SYSTEM", The Journal of neuroscience, 17(22), 1997, pp. 8804-8816

Abstract

Glutamate, the major excitatory neurotransmitter in the CNS, is also an excitatory neurotransmitter in the enteric nervous system (ENS). Wetested the hypothesis that excessive exposure to glutamate, or related agonists, produces neurotoxicity in enteric neurons. Prolonged stimulation of enteric ganglia by glutamate caused necrosis and apoptosis in enteric neurons. Acute and delayed cell deaths were observed. Glutamate neurotoxicity was mimicked by NMDA and blocked by the NMDA antagonist D-2-amino-5-phosphonopentanoate. Excitotoxicity was more pronounced in cultured enteric ganglia than in intact preparations of bowel, presumably because of a reduction in glutamate uptake. Glutamate-immunoreactive neurons were found in cultured myenteric ganglia, and a subsetof enteric neurons expressed NMDA (NR1, NR2A/B), AMPA (GluR1, GluR2/3), and kainate (GluR5/6/7) receptor subunits. Glutamate receptors wereclustered on enteric neurites. Stimulation of cultured enteric neurons by kainic acid led to the swelling of somas and the growth of varicosities (''blebs'') on neurites. Blebs formed close to neurite intersections and were enriched in mitochondria, as revealed by rhodamine 123 staining. Kainic acid also produced a loss of mitochondrial membrane potential in cultured enteric neurons at sites where blebs tended to form. These observations demonstrate, for the first time, excitotoxicityin the ENS and suggest that overactivation of enteric glutamate receptors may contribute to the intestinal damage produced by anoxia, ischemia, and excitotoxins present in food.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 08:57:02