Gabapentin treatment improves motor coordination in a mice model of progressive ataxia

Autor: G. D’Intino, Marco Gusciglio, Alessandro Massella, Luca Ferraro, Sandra Sivilia, Luciana Giardino, Laura Calzà
Přispěvatelé: Massella A., D’Intino G., Gusciglio M., Sivilia S., Ferraro L., Calzà L., Giardino L.
Rok vydání: 2009
Předmět:
Ataxia
Movement disorders
Potassium Channels
Gabapentin
Cyclohexanecarboxylic Acids
Cyclic Nucleotide-Gated Cation Channels
Cell Count
Neurological disorder
HCN1 mice
Rotarod performance test
Mice
Cerebellum
medicine
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
Animals
RNA
Messenger
Amines
Molecular Biology
Motor skill
Chromatography
High Pressure Liquid
gamma-Aminobutyric Acid
Mice
Knockout
Analysis of Variance
Staining and Labeling
Glutamate Decarboxylase
Reverse Transcriptase Polymerase Chain Reaction
General Neuroscience
Age Factors
Motor control
medicine.disease
Motor coordination
GABA content
Disease Models
Animal
Motor Skills
Rotarod Performance Test
Neurology (clinical)
medicine.symptom
Atrophy
Psychology
Neuroscience
Excitatory Amino Acid Antagonists
Developmental Biology
medicine.drug
Zdroj: Brain research. 1301
ISSN: 1872-6240
Popis: No causal treatment of ataxias is available at the moment, and so symptomatic and disease-modifying therapies are regarded as a reliable possibility for this complex group of movement disorders. In order to explore possible pharmacological strategies aimed at interfering with ataxia development or progression, we used HCN1-/- mice. Mice carrying the deletion of the gene encoding for the voltage-dependent K-channel (HCN1-/-) have a normal basic motor function, but impaired learning of the motor skills that enable mice to balance on the rotating rod. In this study we showed that the motor coordination impairment observed in HCN1-/- mice is paralleled by a decline of GABA content in the cerebellum. Treatment with the GABA mimetic gabapentin at prenatal age prevents full development of the ataxia symptom. This result could have implications for possible therapeutic strategies aimed at more effective coupling with ataxia in several neurological diseases in which this symptom develops and is prominent over time. In view of its long-lasting effect, it could be also considered as a disease-modifying drug.
Databáze: OpenAIRE
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