Modification of the natural progression of epileptogenesis by means of biperiden in the pilocarpine model of epilepsy

Date
2017Author
Bittencourt, Simone [UNIFESP]
Ferrazoli, Eneas [UNIFESP]
Valente, Maria Fernanda [UNIFESP]
Romariz, Simone [UNIFESP]
Janisset, Nilma R. L. L. [UNIFESP]
Macedo, Carlos Eduardo [UNIFESP]
Antonio, Bruno de Brito [UNIFESP]
Barros, Vanessa [UNIFESP]
Mundim, Mayara [UNIFESP]
Porcionatto, Marimelia [UNIFESP]
Aarão, Mayra Consuelo
Miranda, Maisa Ferreira
Rodrigues, Antonio Marcio
Guimaraes de Almeida, Antonio-Carlos
Longo, Beatriz M. [UNIFESP]
Mello, Luiz E. [UNIFESP]
Type
ArtigoISSN
0920-1211Is part of
Epilepsy ResearchDOI
10.1016/j.eplepsyres.2017.10.019Metadata
Show full item recordAbstract
Brain injuries are often associated with the later development of epilepsy. Evidence suggests that morphological and functional changes occur in the remaining neural tissue during a silent (or latent) period in which no seizures are expressed. It is believed that this silent (reorganization) period may provide a therapeutic window for modifying the natural history of disease progression. Here we provide evidence that biperiden, a muscarinic anticholinergic agent, is able to alter disease progression in an animal model of epilepsy. We observed that biperiden was capable of slowing the manifestation of the first spontaneous epileptic seizure and effectively reduced the severity and number of recurrent, spontaneous epileptic seizures during the animals' lifespan. Biomolecular (microdialysis) and electrophysiological (extracellular field recordings) studies determined that biperiden was capable of elevating the threshold of hippocampal excitability, thereby making the hippocampal glutamatergic pathways less responsive to stimuli when high concentrations of potassium were used in vivo or in vitro. Notably, there was no hindrance of long-term memory or learning (a potential problem given the amnestic nature of biperiden). We conclude that biperiden has antiepileptogenic potential and may represent an opportunity for the prevention of post-traumatic epilepsy.
Citation
Epilepsy Research. Amsterdam, v. 138, p. 88-97, 2017.Keywords
Disease modifying agentsAnti-epileptogenesis
Symptomatic epilepsies
Neuronal plasticity
Anticholinergic drugs
Sponsorship
CNPqCAPES
FAPEMIG
FAPESP/CInAPCe
Collections
- EPM - Artigos [17701]
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