Abstract
The systemic administration of a potent muscarinic agonist pilocarpine in rats promotes sequential behavioral and electrographic changes that can be divided into 3 distinct periods: (a) an acute period that built up progressively into a limbic status epilepticus and that lasts 24 h, (b) a silent period with a progressive normalization of EEG and behavior which varies from 4 to 44 days, and (c) a chronic period with spontaneous recurrent seizures (SRSs). The main features of the SRSs observed during the long-term period resemble those of human complex partial seizures and recurs 2-3 times per week per animal. Therefore, the pilocarpine model of epilepsy is a valuable tool not only to study the pathogenesis of temporal lobe epilepsy in human condition, but also to evaluate potential antiepileptogenic drugs. This review concentrates on data from pilocarpine model of epilepsy.
Highlights
Epilepsy is the most common serious neurological condition and approximately 50 million people worldwide have it (Sander 2003)
This protein showed its levels increased in the inner molecular layer of the dentate gyrus, during the acute, silent and chronic period, in rats submitted to pilocarpine-induced epilepsy (Naffah-Mazzacoratti et al 1999a)
Trying to understand the role of kinin B1 and B2 receptors in the physiopathology of temporal lobe epilepsy, we developed the epilepsy model induced by pilocarpine in B1 and B2 knockout mice (B1KO and B2KO, respectively), and behavior parameters, cell death and mossy fiber sprouting were analyzed
Summary
The sequential pattern of electrographic changes during the acute phase, immediately following the injection of pilocarpine, is characterized by a significant theta rhythm that replaces the background activity in the hippocampus and low voltage fast activity in the cortex. Growth factors can be released and the activation of their receptors induces the auto-phosphorylation of these receptors and activation of different kinase proteins, including the phosphorylation of proteins on tyrosine residues, which are important in cell cycle and intracellular signalling mechanisms These phosphotyrosine proteins (PTyP), of different molecular weight, have been found to be increased in the hippocampus of rats during the early stages of pilocarpine-induced SE (Funke et al 1998), showing that several intracellular events could undergo modifications during long-lasting seizures, mainly in CA3 region. GAP-43 has been related to processes underlying cell proliferation in fetal human brain and is correlated with differentiation and outgrowth of axons This protein showed its levels increased in the inner molecular layer of the dentate gyrus (regions associated with the mossy fiber sprouting), during the acute, silent and chronic period, in rats submitted to pilocarpine-induced epilepsy (Naffah-Mazzacoratti et al 1999a). BK stimulates the MAPK pathway and binds to neurotrophins receptors, perhaps mediating the phosphorylation of proteins on tyrosine residue (PTyP), changing the gene expression and contributing to plasticity found in the epileptic phenomena
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