Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice
Identifieur interne : 002A21 ( PascalFrancis/Corpus ); précédent : 002A20; suivant : 002A22Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice
Auteurs : Hélène Turmel ; Andreas Hartmann ; Karine Parain ; Aicha Doubou ; Anu Srinivasan ; Yves Agid ; Etienne C. HirschSource :
- Movement disorders [ 0885-3185 ] ; 2001.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1-methyl-4-phenylpyridinium (MPP+) may be mediated by caspase-3. To establish whether caspase-3 activation may indeed play a role in an in vivo model of PD, we studied caspase-3 activation in C57B1/6 mice subchronically intoxicated with MPTP. We show that caspase-3 activation peaks early, at days I and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase-3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 01-0333747 INIST |
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ET : | Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice |
AU : | TURMEL (Hélène); HARTMANN (Andreas); PARAIN (Karine); DOUBOU (Aicha); SRINIVASAN (Anu); AGID (Yves); HIRSCH (Etienne C.) |
AF : | INSERM U 289, Hópital de la Salpétrière/Paris/France (1 aut., 2 aut., 3 aut., 4 aut., 6 aut., 7 aut.); IDUN Pharmaceuticals Inc./La Jolla, California/Etats-Unis (5 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 2; Pp. 185-189; Bibl. 17 ref. |
LA : | Anglais |
EA : | In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1-methyl-4-phenylpyridinium (MPP+) may be mediated by caspase-3. To establish whether caspase-3 activation may indeed play a role in an in vivo model of PD, we studied caspase-3 activation in C57B1/6 mice subchronically intoxicated with MPTP. We show that caspase-3 activation peaks early, at days I and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase-3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo. |
CC : | 002B17G |
FD : | Parkinson maladie; Activité enzymatique; Apoptose; Modèle animal; Pathogénie; Souris; Animal; Caspase 3 |
FG : | Rodentia; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Cysteine endopeptidases; Peptidases; Hydrolases; Enzyme |
ED : | Parkinson disease; Enzymatic activity; Apoptosis; Animal model; Pathogenesis; Mouse; Animal |
EG : | Rodentia; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Cysteine endopeptidases; Peptidases; Hydrolases; Enzyme |
SD : | Parkinson enfermedad; Actividad enzimática; Apoptosis; Modelo animal; Patogenia; Ratón; Animal |
LO : | INIST-20953.354000096545190020 |
ID : | 01-0333747 |
Links to Exploration step
Pascal:01-0333747Le document en format XML
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<front><div type="abstract" xml:lang="en">In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>
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<s5>38</s5>
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<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Cysteine endopeptidases</s0>
<s2>FE</s2>
<s5>45</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Cysteine endopeptidases</s0>
<s2>FE</s2>
<s5>45</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Cysteine endopeptidases</s0>
<s2>FE</s2>
<s5>45</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Peptidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="12" i2="X" l="FRE"><s0>Enzyme</s0>
</fC07>
<fC07 i1="12" i2="X" l="ENG"><s0>Enzyme</s0>
</fC07>
<fC07 i1="12" i2="X" l="SPA"><s0>Enzima</s0>
</fC07>
<fN21><s1>232</s1>
</fN21>
</pA>
</standard>
<server><NO>PASCAL 01-0333747 INIST</NO>
<ET>Caspase-3 activation in 1 -methyl-4-phenyl- 1, 2,3,6-tetrahydropyridine (MPTP)-treated mice</ET>
<AU>TURMEL (Hélène); HARTMANN (Andreas); PARAIN (Karine); DOUBOU (Aicha); SRINIVASAN (Anu); AGID (Yves); HIRSCH (Etienne C.)</AU>
<AF>INSERM U 289, Hópital de la Salpétrière/Paris/France (1 aut., 2 aut., 3 aut., 4 aut., 6 aut., 7 aut.); IDUN Pharmaceuticals Inc./La Jolla, California/Etats-Unis (5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2001; Vol. 16; No. 2; Pp. 185-189; Bibl. 17 ref.</SO>
<LA>Anglais</LA>
<EA>In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) models of Parkinson's disease (PD), dopaminergic (DA) neurons have been shown to die by apoptosis. Moreover, recent postmortem and in vitro results have indicated that apoptotic cell death induced by 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>
) may be mediated by caspase-3. To establish whether caspase-3 activation may indeed play a role in an in vivo model of PD, we studied caspase-3 activation in C57B1/6 mice subchronically intoxicated with MPTP. We show that caspase-3 activation peaks early, at days I and 2 after the end of MPTP intoxication. In contrast, pycnotic neurons persist until day 7 postintoxication, indicating that caspase-3 activation is an early and transient phenomenon in apoptotic death of DA neurons. We further demonstrate that loss of tyrosine hydroxylase (TH) immunoreactivity in this model is indeed due to cell loss rather than to loss of TH protein expression. We conclude that mice subchronically intoxicated with MPTP represent a valid PD model to study and manipulate caspase activation in vivo.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Activité enzymatique; Apoptose; Modèle animal; Pathogénie; Souris; Animal; Caspase 3</FD>
<FG>Rodentia; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Cysteine endopeptidases; Peptidases; Hydrolases; Enzyme</FG>
<ED>Parkinson disease; Enzymatic activity; Apoptosis; Animal model; Pathogenesis; Mouse; Animal</ED>
<EG>Rodentia; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Cysteine endopeptidases; Peptidases; Hydrolases; Enzyme</EG>
<SD>Parkinson enfermedad; Actividad enzimática; Apoptosis; Modelo animal; Patogenia; Ratón; Animal</SD>
<LO>INIST-20953.354000096545190020</LO>
<ID>01-0333747</ID>
</server>
</inist>
</record>
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