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Titolo:
Neuroprotective properties of 17 beta-estradiol, progesterone, and raloxifene in MPTP C57Bl/6 mice
Autore:
Callier, S; Morissette, M; Grandbois, M; Pelaprat, D; Di Paolo, T;
Indirizzi:
Univ Laval, Med Ctr, Oncol & Mol Endocrinol Res Ctr, Quebec City, PQ G1V 4G2, Canada Univ Laval Quebec City PQ Canada G1V 4G2 Quebec City, PQ G1V 4G2, Canada Univ Laval, Fac Pharm, Quebec City, PQ G1V 4G2, Canada Univ Laval Quebec City PQ Canada G1V 4G2 Quebec City, PQ G1V 4G2, Canada Hop St Antoine, INSERM, U339, F-75012 Paris, France Hop St Antoine ParisFrance F-75012 INSERM, U339, F-75012 Paris, France
Titolo Testata:
SYNAPSE
fascicolo: 2, volume: 41, anno: 2001,
pagine: 131 - 138
SICI:
0887-4476(200108)41:2<131:NPO1BP>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
DOPAMINE UPTAKE SITES; PARKINSONS-DISEASE; OVARIECTOMIZED RATS; ESTROGEN-RECEPTOR; OXIDATIVE STRESS; SUBSTANTIA-NIGRA; BRAIN DOPAMINE; CELL-DEATH; INDUCED NEUROTOXICITY; GENDER DIFFERENCES;
Keywords:
dopamine transporter; glutamate; steroid; selective estrogen receptor modulator;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Di Paolo, T Univ Laval, Med Ctr, Oncol & Mol Endocrinol Res Ctr, 2705 Laurier Blvd, Quebec City, PQ G1V 4G2, Canada Univ Laval 2705 Laurier Blvd Quebec City PQ Canada G1V 4G2 ada
Citazione:
S. Callier et al., "Neuroprotective properties of 17 beta-estradiol, progesterone, and raloxifene in MPTP C57Bl/6 mice", SYNAPSE, 41(2), 2001, pp. 131-138

Abstract

Previous work from our laboratory showed prevention of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) induced dopamine depletion in striatum of C57Bl/6 mice by 17 beta -estradiol, progesterone, and raloxifene, whereas 17 alpha -estradiol had no effect. The present study investigated the mechanism by which these compounds exert their neuroprotective activity. The hormonal effect on the dopamine transporter (DAT) was examined to probe the integrity of dopamine neurons and glutamate receptors in order to find a possible excitotoxic mechanism. Drugs were injected daily for 5 days before MPTP(four injections, 15 mg/kg ip at 2-h intervals) and drug treatment continued for 5 more days. MPTP induced a decrease of striatal DAT-specific binding (50% of control) and DAT mRNA in the substantia nigra (20% of control), suggesting that loss of neuronal nerve terminals was more extensive than cell bodies. This MPTP-induced decrease of striatal [I-125]RTI-121 specific binding was prevented by 17 beta -estradiol (2 mug/day), progesterone (2 mug/day), or raloxifene (5 mg/kg/day) but not by 17 alpha -estradiol (2 mug/day) or raloxifene (1 mg/kg/day). No treatment completely reversed the decreased levels of DAT mRNA in the substantia nigra. Striatal [I-125]RTI-121 specific binding was positively correlated with dopamine concentrations in intact, saline, or hormone-treated MPTP mice. Striatal NMDA-sensitive [H-3]glutamate or [H-3]AMPA specific binding remained unchanged in intact, saline, or hormone-treated MPTP mice, suggesting the unlikely implication of changesof glutamate receptors in an excitotoxic mechanism. These results show a stereospecific neuroprotection by 17 beta -estradiol of MPTP neurotoxicity, which is also observed with progesterone or raloxifene treatment. The present paradigm modeled early DA nerve cell damage and was responsive to hormones. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 07:36:09