Changes in sensitivity of bilateral medial vestibular nuclear neurons responding to input stimuli during vestibular compensation and the underlying ionic mechanism.
- Author:
Wei-Xuan XUE
1
;
Qian-Xiao LI
1
;
Yang-Xun ZHANG
1
;
Xiao-Yang ZHANG
1
;
Wing-Ho YUNG
2
;
Jian-Jun WANG
1
;
Jing-Ning ZHU
1
Author Information
1. State Key Laboratory of Pharmaceutical Biotechnology, Department of Physiology, School of Life Sciences, Nanjing University, Nanjing 210023, China.
2. School of Biomedical Sciences, Faculty of Medicine, and Gerald Choa Neuroscience Centre, The Chinese University of Hong Kong, Hong Kong, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Locomotion;
Neurons/physiology*;
Patch-Clamp Techniques;
Rats;
Vestibular Nuclei/metabolism*;
Vestibule, Labyrinth
- From:
Acta Physiologica Sinica
2022;74(2):135-144
- CountryChina
- Language:Chinese
-
Abstract:
Vestibular compensation is an important model for developing the prevention and intervention strategies of vestibular disorders, and investigating the plasticity of the adult central nervous system induced by peripheral injury. Medial vestibular nucleus (MVN) in brainstem is critical center for vestibular compensation. Its neuronal excitability and sensitivity have been implicated in normal function of vestibular system. Previous studies mainly focused on the changes in neuronal excitability of the MVN in lesional side of the rat model of vestibular compensation following the unilateral labyrinthectomy (UL). However, the plasticity of sensitivity of bilateral MVN neurons dynamically responding to input stimuli is still largely unknown. In the present study, by using qPCR, whole-cell patch clamp recording in acute brain slices and behavioral techniques, we observed that 6 h after UL, rats showed a significant deficit in spontaneous locomotion, and a decrease in excitability of type B neurons in the ipsilesional rather than contralesional MVN. By contrast, type B neurons in the contralesional rather than ipsilesional MVN exhibited an increase in response sensitivity to the ramp and step input current stimuli. One week after UL, both the neuronal excitability of the ipsilesional MVN and the neuronal sensitivity of the contralesional MVN recovered to the baseline, accompanied by a compensation of spontaneous locomotion. In addition, the data showed that the small conductance Ca2+-activated K+ (SK) channel involved in the regulation of type B MVN neuronal sensitivity, showed a selective decrease in expression in the contralesional MVN 6 h after UL, and returned to normal level 1 week later. Pharmacological blockage of SK channel in contralateral MVN to inhibit the UL-induced functional plasticity of SK channel significantly delayed the compensation of vestibular motor dysfunction. These results suggest that the changes in plasticity of the ipsilesional MVN neuronal excitability, together with changes in the contralesional MVN neuronal sensitivity, may both contribute to the development of vestibular symptoms as well as vestibular compensation, and SK channel may be an essential ionic mechanism responsible for the dynamic changes of MVN neuronal sensitivity during vestibular compensation.
