Effect of deep brain stimulation on length of dendrites in hippocampal CA1 neurons in pentylenetetrazol kindled rats
نویسندگان
1 Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2 Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3 Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
4 Department of Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
5 Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
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چکیده
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.