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Titolo:
Adenosine prevents the death of mesencephalic dopaminergic neurons by a mechanism that involves astrocytes
Autore:
Michel, PP; Marien, M; Ruberg, M; Colpaert, F; Agid, Y;
Indirizzi:
Hop La Pitie Salpetriere, INSERM, U289, F-75654 Paris 13, France Hop La Pitie Salpetriere Paris France 13 U289, F-75654 Paris 13, France Ctr Rech Pierre Fabre, F-81106 Castres, France Ctr Rech Pierre Fabre Castres France F-81106 re, F-81106 Castres, France
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 5, volume: 72, anno: 1999,
pagine: 2074 - 2082
SICI:
0022-3042(199905)72:5<2074:APTDOM>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
MULTIPLE SYSTEM ATROPHY; CENTRAL-NERVOUS-SYSTEM; RAT STRIATUM; CYTOSINE-ARABINOSIDE; PRIMARY CULTURES; BRAIN NEURONS; IN-VITRO; CELLS; ATP; RELEASE;
Keywords:
adenosine; antimitotic agent; ATP; dopaminergic neurons; neuroprotection; Parkinson's disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Michel, PP Hopcea Pitie Salpetriere, INSERM, U289, 47 Blvd Hop, F-75654 Paris 13, Fran Hop La Pitie Salpetriere 47 Blvd Hop Paris France 13 13, Fran
Citazione:
P.P. Michel et al., "Adenosine prevents the death of mesencephalic dopaminergic neurons by a mechanism that involves astrocytes", J NEUROCHEM, 72(5), 1999, pp. 2074-2082

Abstract

The purinergic nucleoside adenosine effectively prevented the death of dopaminergic neurons that occurs spontaneously and progressively in cultures of rat mesencephalon. Adenosine also significantly increased dopamine uptake, attesting to the state of differentiation and functional integrity of theneurons that were rescued. The effects of adenosine were (a) specific to the dopaminergic neurons in these cultures, (b) long-lived, (c) still observed when the treatment was delayed after plating, (d) potentiated by inhibition of adenosine deaminase, and (e) abolished when this enzyme was added inexcess to the culture medium. The action of adenosine was mimicked by 5'-(N-ethylcarboxamido)adenosine and dibutyryl-cyclic AMP, but not by CGS-21680, suggesting the possible involvement of A(2B) subtype purinergic receptors, ATP was also neuroprotective, but its action resulted principally from conversion to adenosine by ectonucleotidases. Several anticancer drugs, including cytosine arabinoside, have been shown previously to prevent apoptosis in cultured dopaminergic neurons by a mechanism that requires the inhibition of proliferating astrocytes. In the presence of adenosine, astrocytes were more differentiated, and their proliferation rate was significantly reduced, suggesting that the neurotrophic effect of the adenine nucleoside resulted also from the repression of the astroglial cells. We did not find evidence of a trophic intermediary in adenosine-treated cultures, however, leading to the hypothesis that limitation of astrocyte replication in itself and/or ensuing changes in the glial phenotype were crucial. Our results suggest that molecules that modulate adenine nucleotide/nucleoside release may beuseful for the treatment of chronic neurodegenerative conditions affectingdopaminergic neurons, such as Parkinson's disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 14:57:50