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Molecular targets related to neuronal plasticity in different experimental models


The epileptic syndrome could be considered as an active process, where 10ng-Iasting seizures are able to produce important brain impact. These brain modifications are the result of a complex biochemical cascade activation, which can modify the gene expression with consequent alteration of receptors, enzyme activities, trophic factors, extracellular matrix as well as the cytoskeleton proteins. These alterations could modify the brain excitability inducing cerebral damage. A reactive gliosis can also be found in the brain after neuronalloss, which can be induced by 10ng-Iasting seizures. Furthermore, a synaptic remodelation also occur generationg excitatory and recurrent neural network, increasing the neuronal activity and contributing to the manteinance of epilepsy. To study the neuroplasticity after brain damage, several epileptic models have been used. The pilocarpine, the kainic acid and kindling are the most used models. The present project was delineated to identify the molecular targets, related to degenerative and regenerative processes following brain injury. For this purpose two experimental models of epilepsy (pilocarpine and kainic acid) will be used. These models will be developed in adult and developing Wistar rats, knockout mice and in a different rodent especie called Proechimys guyannensis, which are animals resistent to the models of temporal lobe epilepsy... (AU)

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