VGCC expression in facial nucleus motoneurons after facial nerve injury in adult rats
10.3969/j.issn.1001-3733.2017.02.005
- VernacularTitle:大鼠面神经损伤后面神经核运动神经元中VGCC表达变化的研究
- Author:
Lili CAO
;
Rongcheng HU
;
Zhenggen PIAO
- Keywords:
Voltage-gated calcium channels (VGCC);
Facial nerve;
Nerve injury;
Motoneuron;
Nerve regeneration
- From:
Journal of Practical Stomatology
2017;33(2):162-167
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression change of voltage-gated calcium channels(VGCC) in the facial nucleus motoneurons of adult rats after facial nerve injury.Methods:The facial motor nucleus was localized by retrograde labeling with a fluorescent dye,Dil,and identified by Nissl staining.The facial nerve injury model was established by amputation of the main trunk of left facial nerve.Exposure of the right facial nerve without nerve transection was used as the control.Rats were sacrificed at 3,7,14 and 28 days after injury respectively(n =10),the brainstem containing facial nucleus were collected,the expression of P/Q,N,L,R-type calcium channel α1A,α1B,α1C and α1E subunits was examined by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR).Results:Immunohistochemistry results show that whereas α1A,α1E subunits levels did not vary compared with control group 3,7,14,28 days after injury(P ＞0.05),α1B and α1C subunits immunoreactivity decreased in the motoneurons after injury,a sharp decrease was detected at 14 days after injury(P ＜ 0.01),thereafter returned to the control level at 28 days after axotomy(P ＞0.05).The expression of α1B and α1C mRNA was down-regulated,especially 14 days after the injury(P ＜0.01),and then recovered to normal level at 28 days (P ＞ 0.05).In addition,there was no significant difference of α1A and α1E subunits and their correspoding mRNA between operated group and control group at all time points(P ＞ 0.05).Conclusion:VGCC is involved in facial nerve injury and down-regulation of N-type and L-type calcium channels may be one of the role.
