The lesional and epileptogenic consequences of lithium-pilocarpine induced status epilepticus are affected by previous exposure to isolated seizures : effects of amygdala kindling and maximal electroshocks

摘要: Abstract In temporal lobe epilepsy, the occurrence of seizures seems to correlate with presence lesions underlying establishment a hyperexcitable circuit. However, in lithium–pilocarpine model neuronal damage occurs both structures belonging circuit initiation and maintenance (forebrain limbic system) as propagation areas (cortex thalamus) remote control (substantia nigra pars reticulata). To determine whether or not we could protect brain from epileptogenesis induced by status epilepticus identify cerebral involved genesis studied effects chronic exposure non-deleterious seizures, either focalized secondary generalization (amygdala kindling, kindled-pilocarpine rats), primary generalized (ear-clip electroshocks, electroshock-pilocarpine rats) on epilepticus. These animals were compared rats subjected but pretreated (sham-kindled-pilocarpine sham-electroshock-pilocarpine rats). Compared sham-pilocarpine rats, was prevented system except hilus dentate gyrus entorhinal cortex, while it enhanced mainly perirhinal cortices. Most sham-kindled- (92–100%) developed recurrent after silent period 40–54 days. Likewise, all spontaneous same latency their sham controls, only two 10 became epileptic delay 106–151 days. The present data show that apparent antiepileptic properties electroshocks extensive midbrain cortical regions, which may prevent hippocampus inhibit motor expression. Conversely, neuroprotection cortex provided amygdala kindling does epileptogenesis. Thus, hilus, and/or be key structure(s) for epilepsy.