| Abstract No.: | B-B2040 |
| Country: | Canada |
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| Title: | INSULAR CORTEX EXCITABILITY AND CHARACTERISATION OF THE EFFECT OF GLUR5 RECEPTORS IN A RODENT MODEL OF TEMPORAL LOBE EPILEPSY |
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| Authors/Affiliations: | 1 Aleksandra Bortel*; 1 Philip de Guzman; 1 Giulia Curia; 1 Massimo Avoli;
1 Montreal Neurological Institute, McGill University, QC, Canada
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| Content: | Objectives: Temporal lobe epilepsy (TLE) is the most common form of human partial complex seizures. Brain from TLE patients presents with mossy fiber sprouting and neuronal loss in different structures. Similar alterations are present in the animal model of TLE induced by systemic injection of pilocarpine. It has been shown that limbic structures are involved in induction and maintenance of seizures in TLE; however, other structures may play a crucial role. Several studies reported that structural and functional changes occur in the insular cortex of TLE patients. There is no data about the changes that appear in the insular cortex in a rat model of TLE. Glutamate mediates fast synaptic transmission through three classes of ionotropic receptors, and relatively little is known about the physiological role of GluR5 receptors that are considered to play a role in triggering seizure discharges. Therefore, we studied the effects of GluR5 receptor activation in insular cortex of rats with TLE.
Materials and methods: We performed field potential and intracellular (sharp-electrode) recordings in pilocaprine-treated and non-epileptic control (NEC) male rats. Animals were injected with scopolamine and 30 min later with pilocarpine (410 mg/kg i.p.). Only rats that experienced status epilepticus for 30 min or more were included in the pilocarpine group and used for in vitro electrophysiological studies. Control animals were injected with scopolamine.
Results: In normal ACSF condition there was no spontaneous field activity in pilocaprine-treated and NEC insular cortex. Upon bath application of the selective GluR5 agonist (3 μM ATPA) the field activity continued to be absent in NEC slices, while 10 μM ATPA generated spontaneous monophasic field potential responses. In contrast, in pilocarpine-treated insular cortex 3 μM ATPA induced spontaneous field potential activity that increased upon higher concentrations of ATPA (10 μM).
Single-shock electrical stimuli delivered in insular cortex elicited bursting responses in 20% of NEC cells and in 90% of pilocarpine-treated neurons. The reversal potentials of postsynaptic events of epileptic neurons were more hyperpolarized compared to control neurons.
Conclusion: Our findings suggest that the insular cortex in the pilocarpine animal model of TLE is hyperexcitable compared to NEC, and that the GluR5 receptor activation induces epileptiform activity in this brain region. |
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