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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