http://orcid.org/0000-0001-9785-8166
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Abstract
Background: Unilateral labyrinthectomy (UL) causes the disappearance of ipsilateral medial vestibular nuclear (ipsi-MVe) activity and induces spontaneous nystagmus (SN), which disappears during the initial process of vestibular compensation (VC). Ipsi-MVe-activity restores in the late process of VC.
Objective: We evaluated the late process of VC after UL in rats and examined the effects of thioperamide (H3 antagonist) on VC.
Materials and methods: MK801 (NMDA antagonist)-induced Fos-like immunoreactive (-LIR) neurons in contra-MVe, which had been suppressed by NMDA-mediated cerebellar inhibition in UL rats was used as an index.
Results: The number of MK801-induced Fos-LIR neurons in contra-MVe gradually decreased to the same level as that of sham-operated rats 14 days after UL. Thioperamide moved the disappearance of the MK801-induced Fos-LIR neurons 2 days earlier. The number of MK801-induced Fos-LIR neurons in thioperamide-treated rats was significantly decreased, compared with that of vehicle rats on days 7 and 12 after UL. But, thioperamide did not influence the decline of SN frequency in UL rats.
Conclusion: These findings suggested that the number of MK801-induced Fos-LIR neurons in contra-MVe was decreased in concordance with the restoration of ipsi-MVe-activity during the late process of VC after UL and that thioperamide accelerated the late, but not the initial process of VC.
Chinese abstract
背景：单侧迷路切除术（UL）导致同侧内侧前庭核（ipsi-MVe）活动消失并诱发自发性眼球震颤（SN）, 后者在前庭补偿（VC）初期消失。 Ipsi-MVe活动在VC后期恢复。
目的：评价大鼠UL后VC的晚期过程, 并检测硫哌酰胺（H3拮抗剂）对VC的影响。
材料和方法：MK801（NMDA拮抗剂）诱导的抗MVe中的Fos样免疫反应性（-LIR）神经元被用作指标；它已经被UL大鼠的NMDA介导的小脑抑制所抑制。
结果：抗MVe中MK801诱导的Fos-LIR神经元数量在UL后14天逐渐下降至与假手术大鼠相同的水平。硫丙使得MK801诱导的Fos-LIR神经元的消失提前了两天。在UL后第7天和第12天, 与载体大鼠相比, 硫丙处理的大鼠中MK801诱导的Fos-LIR神经元的数量显著减少。但是, 硫丙并未影响UL大鼠SN频率的下降。
结论：这些研究结果表明, 在UL之后VC的后期过程中, MV801诱导的Fos-LIR神经元在抗MVe中的数量随着ipsi-MVe活性的恢复而减少, 而且硫丙加速了VC的晚期过程, 而不是它的初始过程。
Disclosure statement
No potential conflict of interest was reported by the authors.
Acknowledgements
The authors thank Professor Bukasa Kalubi for his critical reading of the manuscript.