Expression of Canonical Transient Receptor Potential Channel Protein in the Hippocampus of AmyloidβProtein-induced Alzheimer’s Disease Mice / 中国医科大学学报
Journal of China Medical University
; (12): 1100-1104, 2016.
Article
in Zh
| WPRIM
| ID: wpr-506617
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WPRO
ABSTRACT
Objective To investigate the protein expression of the canonical transient receptor potential(TRPC)channel in the hippocampus of amyloidβprotein(Aβ)?induced Alzheimer’s disease(AD)mice. Methods A total of 36 ICR mice were randomly divided into AD group and control group,with 18 rats in each group. AD mice models were established by Aβ1?42 microinjection into the lateral intracerebroventricular. Learning and memory abilities of the mice were determined using Morris water maze. All TRPC1?TRPC7 mRNA levels in the hippocampus of the mice were detected using reverse transcriptase polymerase chain reaction(RT?PCR). Hippocampal TRPC4 protein expression was examined using immunofluorescence and Western blotting methods. Results Water maze test results showed that the escape latency of AD group were significant?ly longer than that of the control group(P<0.01),and that the target quadrant occupancy of AD group was significantly shortened(P<0.01)and the frequency of platform crossing of AD group was significantly reduced(P<0.01). RT?PCR results showed that all TRPC(TRPC1?TRPC7) mRNA were expressed in the hippocampal of both AD group and control group. Among these channels ,only TRPC4 mRNA levels of AD group was higher than that of the control group(P<0.01). Immunofluorescence images showed that TRPC4 expressed on the membrane of neurons and the intensities of the immunofluorescence of TRPC4 in AD group were stronger than that of control group. Western blotting results showed that the TRPC4 protein expression of AD group was higher than that of control group(P<0.05). Conclusion The increase of TRPC4 protein expression in the hippocampus of mice after intracerebroventricular injection of Aβ1?42 oligomers suggests that TRPC4 may be involved in the pathogenesis of AD induced by calcium homeostasis.
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Language:
Zh
Journal:
Journal of China Medical University
Year:
2016
Type:
Article