Lamotrigine Is Neuroprotective in the Energy Deficiency Model of MPTP Intoxicated Mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-07

AUTHORS

EMMANUELLE LAGRUE, SYLVIE CHALON, SYLVIE BODARD, ELIE SALIBA, PIERRE GRESSENS, PIERRE CASTELNAU

ABSTRACT

The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) inhibits the mitochondrial complex I of the respiratory chain. This results in ATP and ion homeostasis disturbances, which lead to selective death of the substantia nigra dopaminergic neurons. Well known as a Parkinson's disease model, the MPTP animal model also provides a potential paradigm of the energy deficiencies found in childhood. In these conditions, anticonvulsants may provide neuroprotection by limiting cellular energy consumption. We tested valproate, topiramate and lamotrigine in the MPTP mouse model. Dopamine transporter (DAT) density was assessed by quantitative autoradiography, tyrosine hydroxylase (TH) was evaluated by immunohistochemistry and dopamine (DA) levels by HPLC-ED whereas neuronal apoptosis was monitored through active caspase-3. Expectedly, the DAT density, TH immunoreactive neurons and DA content in the MPTP group were respectively reduced to 51%, 40% and 26% versus control animals. Unlike valproate and topiramate, lamotrigine provided a significant neuroprotection against MPTP in maintaining these levels at 99%, 74% and 58% respectively and reducing the induced apoptosis. Altogether, the data indicate that lamotrigine limits dopaminergic neuronal death in the substantia nigra and promotes striatal dendrites sprouting. Lamotrigine, a widely used and well-tolerated molecule in young patients, could represent a valuable adjuvant therapy in various energy deficiency conditions during childhood. More... »

PAGES

14-19

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1203/pdr.0b013e31806790d7

DOI

http://dx.doi.org/10.1203/pdr.0b013e31806790d7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1048842444

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17515828


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26 schema:description The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) inhibits the mitochondrial complex I of the respiratory chain. This results in ATP and ion homeostasis disturbances, which lead to selective death of the substantia nigra dopaminergic neurons. Well known as a Parkinson's disease model, the MPTP animal model also provides a potential paradigm of the energy deficiencies found in childhood. In these conditions, anticonvulsants may provide neuroprotection by limiting cellular energy consumption. We tested valproate, topiramate and lamotrigine in the MPTP mouse model. Dopamine transporter (DAT) density was assessed by quantitative autoradiography, tyrosine hydroxylase (TH) was evaluated by immunohistochemistry and dopamine (DA) levels by HPLC-ED whereas neuronal apoptosis was monitored through active caspase-3. Expectedly, the DAT density, TH immunoreactive neurons and DA content in the MPTP group were respectively reduced to 51%, 40% and 26% versus control animals. Unlike valproate and topiramate, lamotrigine provided a significant neuroprotection against MPTP in maintaining these levels at 99%, 74% and 58% respectively and reducing the induced apoptosis. Altogether, the data indicate that lamotrigine limits dopaminergic neuronal death in the substantia nigra and promotes striatal dendrites sprouting. Lamotrigine, a widely used and well-tolerated molecule in young patients, could represent a valuable adjuvant therapy in various energy deficiency conditions during childhood.
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34 DA content
35 DAT density
36 Energy Deficiency Model
37 HPLC-ED
38 MPTP
39 MPTP animal model
40 MPTP group
41 MPTP intoxicated mice
42 MPTP mouse model
43 Parkinson's disease model
44 TH immunoreactive neurons
45 active caspase-3
46 adjuvant therapy
47 animal models
48 animals
49 anticonvulsants
50 apoptosis
51 autoradiography
52 caspase-3
53 cellular energy consumption
54 chain
55 childhood
56 complex I
57 conditions
58 consumption
59 content
60 control animals
61 data
62 death
63 deficiency
64 deficiency conditions
65 deficiency model
66 density
67 disease models
68 disturbances
69 dopamine levels
70 dopamine transporter density
71 dopaminergic neuronal death
72 dopaminergic neurons
73 energy consumption
74 energy deficiency
75 energy deficiency conditions
76 group
77 homeostasis disturbance
78 hydroxylase
79 immunohistochemistry
80 immunoreactive neurons
81 intoxicated mice
82 ion homeostasis disturbances
83 lamotrigine
84 levels
85 mice
86 mitochondrial complex I
87 model
88 molecules
89 mouse model
90 neuronal apoptosis
91 neuronal death
92 neurons
93 neuroprotection
94 nigra
95 nigra dopaminergic neurons
96 paradigm
97 patients
98 potential paradigm
99 quantitative autoradiography
100 respiratory chain
101 selective death
102 significant neuroprotection
103 striatal
104 substantia nigra
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106 therapy
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108 tyrosine hydroxylase
109 valuable adjuvant therapy
110 younger patients
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