Influence On The Insular Function And Structure Of The Epilepsy

Part one：Epilepsy affected the island lobe brain regions GABAneuron subtypes expressIsland leaves the fifth lobe of the human brain, is located in the temporal lobe,frontal, top island deep cover. The study of the island affected in the process of epilepsy isless known. The study found that temporal lobe epilepsy, many patients with temporallobe epilepsy that the insular cortex may cause seizures, but the insular cortex in thisprocess will play what role is unknown.Our study’s object is the GABA neurons in the insular cortex，observation afterseizures different subtypes of GABA neurons in the insular cortex changes, and with thehippocampus to compare. By immunohistochemical staining method compares theexpress changes in the insular cortex and hippocampus of two GABA neuron subtypes PVand SST，found the normal island PV expressed strong,3days and30days afterepilepsy the PV expressed significantly weakened, reducing the number of positive cellseither.3days after epilepsy SST staining significantly strengthened and30days after theepilepsy cells became round, the number of SST strongly positive cells increased, anddendritic staining intensity is also increased. In the hippocampal has the opposite trendcompared with the insular cortex，PV staining in3days and30days has a strong upwardtrend, while weakening trend in SST.Through our research, it is found that the insular cortex and hippocampus brainregions after epilepsy GABA neurons change just showed the opposite trend, suggestingthat the insular cortex may plays a secondary epileptic foci of spontaneous seizures inepilepsy secondarythe role, which is consistent with clinical observations. Its mechanismneeds further study. Part two:Epilepsy affected the insular cortex Stathmin protein expression and microtubule stabilityPatients with temporal lobe epilepsy have inexplicable fear attack as the aurasymptoms. Contextual fear conditioning in rats was impaired in both pilocarpine and kanicacid model of epilepsy. However, seizure-modulated fear and the underlying basics ofneuronal mechanisms remain unclear. Recent studies identified stathmin as one of the keymolecules controlling both learned and innate fear. Stathmin binds to tubulin and inhibitsmicrotubule assembly and promotes microtubule catastrophes. Therefore we predict thatstathmin play the crucial role in associating the two processes, epilepsy seizures and fearconditioning. We first established pilocarpine model of epilepsy in rats, and then make thefear condition training with the epilepsy rats. Rats of the epilepsy plus fear conditioning(epilepsy+fear) have a much longer freezing time than the single fear or epilepsy groups.The increased freezing levels revealed a significant strengthen effect of epilepsy seizureson the learned fear of the tone-shock contextual. We then compared the stathminexpression in the hippocampus, the amygdale, the insular cortex and the temporal lobe.We found that the dramatic change of stathmin expression happened in the insular and inthe hippocampus but not in the amygdale. We compared the stathmin expression and thedendritic microtubule stability between fear and epilepsy rats. We found that epilepsy canstrengthen the fear conditioning with increased expression of stathmin and decreasedmicrotubule stability. Fear conditioning increased the expression of stathmin slightly whilethe epilepsy plus fear increased it dramatically in the hippocampus, insular cortex andhypothalamus. The phosphorylated stathmin slightly increased in the epilepsy plus fearconditioning rats. The increased expression of stathmin was inversely correlated with thedecrease of the stathmin MAP2and α-tubulin in the epilepsy plus fear groups in all threebrain areas. The most dramatic change of the ratio of MAP2and α-tubulin/stathminhappened in the insular cortex and hippocampus. We conclude that epilepsy can strengthenthe fear conditioning with the increased stathmin and decreased microtubule stability,especially in the insular cortex and hippacampus. We proposed that the insular cortex may play a more important role when considered the correlation of fear and epilepsy.