Caspase‐3 activation in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mice
Identifieur interne : 004850 ( Main/Curation ); précédent : 004849; suivant : 004851Caspase‐3 activation in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mice
Auteurs : Hélène Turmel [France] ; Andreas Hartmann [France] ; Karine Parain [France] ; Aicha Douhou [France] ; Anu Srinivasan [États-Unis] ; Yves Agid [France] ; Etienne C. Hirsch [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2001-03.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (administration & dosage), 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Animal, Animal model, Animals, Apoptosis, Apoptosis (drug effects), Caspase 3, Caspases (metabolism), Disease Models, Animal, Dopamine Agents (administration & dosage), Dopamine Agents (adverse effects), Enzymatic activity, Immunohistochemistry, MPP+, MPTP, Male, Mice, Mice, Inbred C57BL, Mouse, Neurons (drug effects), Neurons (enzymology), Neurons (pathology), Parkinson Disease, Secondary (chemically induced), Parkinson disease, Parkinson's disease, Pathogenesis, Substantia Nigra (drug effects), Substantia Nigra (enzymology), Tyrosine 3-Monooxygenase (metabolism), apoptosis, caspase‐3.
- MESH :
- chemical , administration & dosage : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Dopamine Agents.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Apoptosis, Neurons, Substantia Nigra.
- enzymology : Neurons, Substantia Nigra.
- chemical , metabolism : Caspases, Tyrosine 3-Monooxygenase.
- pathology : Neurons.
- Animals, Caspase 3, Disease Models, Animal, Immunohistochemistry, Male, Mice, Mice, Inbred C57BL.
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 C57Bl/6 mice subchronically intoxicated with MPTP. We show that caspase‐3 activation peaks early, at days 1 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. © 2001 Movement Disorder Society.
Url:
DOI: 10.1002/mds.1037
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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+) 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 C57Bl/6 mice subchronically intoxicated with MPTP. We show that caspase‐3 activation peaks early, at days 1 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. © 2001 Movement Disorder Society.</div>
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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+) 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 C57Bl/6 mice subchronically intoxicated with MPTP. We show that caspase‐3 activation peaks early, at days 1 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. © 2001 Movement Disorder Society.</div>
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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(+)) 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 C57Bl/6 mice subchronically intoxicated with MPTP. We show that caspase-3 activation peaks early, at days 1 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.</div>
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