Abstract
Objective To study the relationship of BDNF - TrkB signaling pathway and the expression of Arc in amygdala electrical stimulation kindled rats and the epilepsy.Methods Male SD rats were divided randomly into control group,sham group and amygdala kindled group (simple kindling group,k252a injection group,DMSO control group).Application of Alpha - Lab 4 channel signal acquisition and processing system recording the EEG activity of rats.The expression level of Arc gene in hippocampus was test by RT - PCR and hybridization,The expression level of Arc protein was test by immunohistochemistry.Results The V class insultus duration of k252a injection group rats (33.00 ± 1.41 )s,they were significantly less than the simple kindling group rats(60.50 ± 2.07) s and the DMSO control group rats(60.00 ± 1.79) s( P ＜0.01 ).The Arc of positive cells percentage was significantly lower at 3 h,6 h in k252a injection group than simple kinding group,DMSO control group( P ＜ 0.01 ).The expression of Arc positive cells percentage among 5 groups at 12 h was no statistically significant ( F =0.684,P ＞ 0.05 ).The resulted of RT - PCR,hybridization showing:The expression of Arc mRNA at 1 h,3 hsignificantly lower in k252a injection group than simple kinding group,DMSO control group( P ＜ 0.01 )The defference of expression of Arc mRNA at 6 h among 5 groups was no statistically significant ( P ＞0.05 ).Conclusion k252a can inhibiting BDNF- TrkB signaling pathyway inducing the expression of Arc,to reduce the duration of seizure. Key words: Amygadala; Epilepsy; Activity-regulated cytoskeletal protein; k252a; Brain-derived neurotrophic factor
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
