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Electrical Kindling is one of the most popular epileptic model techniques that cause seizures such as temporal lobe epilepsy. So far, various therapies have been used to treatment of epilepsy. Among these treatments, low-frequency stimulation (LFS) has been widely considered for improving effect on drug-resistant epilepsy, but its mechanism is not well understood. Since calcium entering to the cytoplasm and increasing its concentration is one of the reasons for seizure, metabotropic glutamate receptor (mGluR1), dopamine receptor (D1) and ADPR cyclase (CD38), which increased calcium in the cytoplasm from different pathways, were selected. With this aim that by examining the change in the expression of these genes, we help to clarify the LFS improvement effect.  In this study, the hippocampus of rats was used and the changes in genes expression were investigated using real-time PCR technique. The results showed that the expression of all selected genes  increased significantly after kindling and then after the LFS the expression of all was returned to sham value. Hence, one of the ways in which LFS interferes may be related to the pathway for calcium entering to the cytoplasm.

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Aim: Applying deep brain stimulation at low-frequency has anticonvulsant effect on kindled seizures. In this study, the effect of low-frequency stimulation (LFS) on kindling-induced changes in the dendritic length of hippocampal CA1 neurons was investigated.
Methods: To administer LFS in the hippocampus, animals first underwent stereotactic surgery and a tripolar electrode were positioned in the CA1 region. Animals received intraperitoneal pentylenetetrazole (PTZ; 34 mg/kg) every other day until they showed three consecutive stage 4 or 5 seizures. LFS was administered to the dorsal hippocampal CA1 area in kindled+LFS group. Hippocampal samples were prepared for stereological assessment one week after termination of LFS application.
Results: PTZ kindling was accompanied with a decrease in dendritic length in CA1 neurons. One week after application of LFS, the length of dendrites was restored to control group values, and there was a significant difference between kindled+LFS and kindled groups. Interestingly, the effect of administering LFS alone in control group, was similar to that of kindled group and a significant decrease was observed in dendritic length.
Conclusion: LFS had a restoring effect on morphological changes in CA1 neurons of kindled animals. This effect may be considered a mechanism for therapeutic action of deep brain stimulation in seizure.

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low-frequency electrical stimulation (LFS) has been considered as a new treatment method for epilepsy patients resistant to drug treatment, but its mechanism of action is not fully understood. Gi protein-coupled receptors such as dopamine D2-like receptors may play a role in mediating the effects of LFS. In this study, the role of dopamine D2-like receptors in the effects of LFS on seizure-induced spontaneous synaptic activity in the hippocampal CA1 region of fully kindled rats has been investigated. Animals were kindled by semi-rapid kindling method (6 stimulations per day) by electrical stimulation of the hippocampal CA1 region. In LFS-treated groups, animals received 4 LFS packets at 5 minutes, 6 hours, 24 hours, and 30 hours after the last LFS stimulation.Each LFS package consisted of 4 series with an interval of 5 minutes, and each series consisted of 200 pulses, and the pulse duration was 0.1 ms with a frequency of 1 Hz. Haloperidol (D2 receptor antagonist, mµ2) or bromocriptine (D2 receptor agonist, g/µlitµ2) was injected into the lateral ventricle immediately after the last kindling stimulation, before applying LFS. The obtained results showed that the application of LFS in kindled animals did not affect the spontaneous excitatory currents in the hippocampus, but it caused a decrease in the spontaneous inhibitory currents in the hippocampus. D2 receptor agonist did not mimic the effects of LFS. The use of haloperidol did not affect the effects of LFS. Therefore, spontaneous excitatory and inhibitory potentials are not a suitable quantity to investigate the effectiveness of LFS.