迷路损伤增强大鼠前庭内侧核生长相关蛋白mRNA水平

前庭代偿是研究神经可塑性的一个理想模型。生长相关蛋白（ＧＡＰ－４３）在神经再生和突触重组中起重要作用。用ＤＩＧ标记的ＧＡＰ－４３ ｃＤＮＡ片段作探针进行原位杂交,检测了大鼠迷路损伤５、１２、２０和３０ｄ后前庭内侧核ＧＡＰ－ｍＲＮＡ表达的变化。结果表明,迷路损毁后两侧前庭内侧核ＧＡＰ－４３ｍＲＮＡ的水平以不同的幅度和时程明显升高。这一结果表示,ＧＡＰ－４３ｍＲＮＡ水平的提高可能与前庭代偿中突触重组和     

原位杂交检测大鼠前庭代偿中GAP-43 mRNA水平

用ＤＩＧ标记的ＧＡＰ－４３ｃＤＮＡ为探针,以大鼠海马切片作阳性对照,使用原位杂交方法检测了大鼠迷路损毁５,１２,２０和３０ｄ后前庭核区ＧＡＰ－４３ｍＲＮＡ水平的变化,结果表明,迷路损毁后前庭核区ｍＲＮＡ水平升高,原位杂交的应用,为前庭代偿中轴突发芽,突触重组的神经可塑性研究打下了方法学基础。     

Acetyl—DL—leucine对猫单侧前庭神经切断后运动平衡能力和前庭外…

本文观测了Ａｃｅｔｙｌ－ＤＬ－ｌｅｕｃｉｎｅ对猫单侧前庭神经切断后前庭代偿的影响。结果显示;ＡＬ加快术后猎在转动横梁测试中运动平衡能力的恢复,但抑制去传入前庭外侧核神经元静息自发放电频率的恢复。ＡＬ促进放电活动与头部左右动体位相关的神经元数量和比例的恢复,从术后的第１周的１０％,逐渐提高到术后第３周的６０％。第５周的７５％。     

Acetyl-DL-leucine对猫单侧前庭神经切断后运动平衡能力和前庭外侧核神经元放电活动恢复的影响

本文观测了Ａｃｅｔｙｌ－ＤＬ－ｌｅｕｃｉｎｅ（ＡＬ、一种抗眩晕药）对猫单侧前庭神经切断后前庭代偿的影响。结果显示：ＡＬ加快术后猫在转动横梁测试中运动平衡能力的恢复,但抑制去传入前庭外侧核神经元（ｎ＝５０６）静息自发放电频率的恢复。ＡＬ促进放电活动与头部左右摆动体位相关的神经元数量和比例的恢复,从术后的第１周的１０％（ｎ＝４５４）,逐渐提高到术后第３周的６０％,第５周的７５％     

前庭代偿中双侧前庭内侧核对输入刺激响应的敏感性变化及其离子机制

前庭代偿是研究前庭疾病防治策略和成年后由外周损伤导致的中枢神经系统可塑性的重要模型。脑干中的前庭内侧核(medial vestibular nucleus, MVN)是实现前庭代偿的重要中枢。MVN神经元的兴奋性和敏感性对前庭功能的正常执行十分关键,但先前的研究集中关注于单侧外周迷路切除(unilateral labyrinthectomy, UL)这一前庭代偿模型中患侧MVN中神经元兴奋性活动的变化,对双侧MVN神经元动态响应输入刺激的敏感性变化仍知之甚少。本研究采用实时荧光定量PCR、离体脑片全细胞膜片钳记录和行为学方法,观察到UL后6 h,大鼠表现出显著的自发运动障碍,且其患侧而非健侧MVN中B型神经元的兴奋性活动显著降低。但与之相反,健侧而非患侧MVN中的B型神经元对斜坡和阶跃电流刺激的敏感性则显著升高。UL后1周,大鼠基础运动行为得到代偿,其患侧MVN神经元的兴奋性和健侧MVN神经元的敏感性均恢复至正常水平。此外,参与B型MVN神经元敏感性调控的小电导钙激活钾通道(small conductance Ca2+-activated K+channel, SK) UL后6 h在健...     

前庭功能的中枢组胺能神经调制

组胺能药物已经长期用于治疗人类的平衡紊乱,但对于它们在前庭系统中作用的机制还缺乏了解。在本文中,我们综述了关于脑内（特别是脑干前庭核中）的组胺能神经传递,以及组胺在脑可塑性——“前庭代偿”（一种单侧外周前庭损伤之后发生的行为学恢复）中作用的新近文献。我们在综述组胺能类药物促进前庭代偿证据的同时,也讨论了这类药物临床应用的可能性。     

多感觉在姿势控制中的作用

姿势控制参与了日常生活的各个方面,能够维持身体平衡,防止跌倒的发生。本文从姿势控制的定义入手,分析视觉、前庭觉和本体感觉作用于姿势控制的途径,以及各感觉受损后姿势控制的代偿现象。通过文献研究法,本文得出姿势控制不仅是应对姿势扰动的反射活动,也包含了在空间中的定向能力,为主动活动提供最佳身体对线;作用于姿势控制的视觉途径包括通过视力、对比敏感度、视野与立体视觉,前庭觉途径包括前庭感受器与前庭反射,本体感觉途径包括本体感受器与中枢处理能力。总体而言,一种感觉成分受损后,机体能够通过另外两种感觉代偿,各感觉具体的代偿方式不一。     

原位杂交检测大鼠前庭代偿中GAP-43 mRNA水平

用DIG标记的GAP-43 cDNA为探针,以大鼠海马切片作阳性对照,使用原位杂交方法检测了大鼠迷路损毁5、12、20和30 d后前庭核区GAP-43 mRNA水平的变化.结果表明,迷路损毁后前庭核区mRNA水平升高.原位杂交的应用,为前庭代偿中轴突发芽,突触重组的神经可塑性研究打下了方法学基础.     

单侧迷路破坏后大鼠前庭神经内侧核区氨基酸含量的变化

本实验用脑部微量透析法和高效液相色谱法观察单侧迷路破坏(unilateral labyrinthectomy,经利多卡因或对氨基苯胂酸盐预处理以阻断单侧外周前庭器官)后大鼠同侧及对侧前庭神经内侧核(medial vestibular nucleus,MVN)区部分氨基酸(天冬氨酸、谷氨酸、谷氨酰胺、甘氨酸、牛磺酸和丙氨酸)含量的变化,以了解前庭代偿的部分神经化学机制.实验观察到,对照组大鼠MVN区天冬氨酸、谷氨酸、谷氨酰胺、甘氨酸、牛磺酸和丙氨酸浓度分别为(6.15±0.59),(18.13±1.21),(33.73±1.67),(9.26±0.65),(9.56±0.77)和(10.07±0.83)pmol/8 μL透析样本.左侧中耳内灌注2%利多卡因后10 min,同侧MVN区天冬氨酸、谷氨酸含量立即减少(P＜0.05),牛磺酸含量增加(P＜0.05);对侧MVN区谷氨酸含量立即增加(P＜0.05),甘氨酸和丙氨酸含量减少;双侧核团间谷氨酸、甘氨酸和丙氨酸含量失衡.而用对氨基苯胂酸盐永久阻断单侧前庭器官2周后,同侧MVN区谷氨酸和丙氨酸含量减少,谷氨酰胺含量增高;对侧MVN区谷氨酸含量也减少;同侧MVN区谷氨酰胺含量明显高于对侧MVN区.结果提示,单侧迷路破坏后双侧MVN区氨基酸含量立即失去平衡,随着前庭代偿的进展,此差异减少,但是在前庭代偿后却出现双侧前庭核区谷氨酰氨的含量失衡,说明在前庭代偿过程中氨基酸含量变化起着重要作用.     

KF核及B(o)tzinger复合体内GABA能神经元向膈神经核的投射

实验在６只成年猫上进行。将ＷＧＡ－ＨＲＰ微量注入Ｃ５膈神经核内,通过逆行追踪及ＧＡＢＡ免疫组织化学ＦＩＴＣ荧光双重标记方法,研究了脑干内ＧＡＢＡ能神经元向膈神经核的投射。结果在脑桥ＫＦ核和面神经后核周围区（即Ｂｏｔｚｉｎｇｅｒ复合体）观察到ＧＡＢＡ－ＨＲＰ双标神经元。另外,在中缝大核、旁巨细胞外侧核及前庭神经核也观察到双标神经元。本实验结果表明：发自上述脑干神经核团,特别是ＫＦ核及Ｂｏｔｚｉｎｇｅ     

A neural network simulation of the vestibular system: implications on the role of intervestibular nuclear coupling during vestibular compensation

 Previous neural network simulations of the vestibular system have been based loosely on known physiology. This research involved the use of a strongly physiologically based neural network model which was used to investigate the role of the vestibular commissure in restoring the bilateral symmetry of the resting rates of the vestibular nuclei during vestibular compensation following unilateral labyrinthectomy. It was found that readjustments in the gain of the vestibular commissure were not primarily responsible for vestibular compensation, as has previously been suggested, but rather that it was modifications in extralabyrinthine sources of tone which mediated the restoration of the central symmetry between the two nuclei. Received: 20 November 1995/Accepted in revised form: 24 July 1996     

Rotations in a vertebrate setting: evaluation of the symmetry group of the disynaptic canal-neck projection

Organizational structures intrinsic to nervous systems can be more precisely analyzed and compared with other logical structures once they are expressed in mathematical languages. A standard mathematical language for expressing organizational structure is that of groups. Groups are especially well suited to organizational structures involving multiple symmetries such as spatial structures. The vestibular system is widely believed to mediate many neural functions involving spatial structure. The vestibular nuclei receive direct projections from the vestibular endorgans, the semicircular canals and the otolith organs. The near-orthogonal directions of the semicircular canals are embedded in the bone. However, those canal directions are external to the nervous system. This study addresses the way the three-dimensional space of rotations is also embedded in the group structure of neural connectivity. Although we know a great deal about physical rotation, it is not clear that nervous systems organize rotations in the same way as physicists do. It would make sense for nervous systems to organize rotations in such a way as to provide physiologically relevant information about performing or compensating for rotations. The vestibular nuclei, which might be expected to display an organization that binds rotations into a rotation space, do not give a clear organization. This may be because of the multiplicity of spatial functions performed by the vestibular nuclei; rather than one spatial organization, the vestibular nuclei are likely to accommodate multiple, related spatial organizations. This study evaluates one particular data set from the literature that specifies the organization of the disynaptic canal-neck projection; other projections and neuronal populations may have other intrinsic organizations. The data are evaluated directly for their symmetry group. In the symmetry group, the vertebrate requirement that physiology have a right and left is found to be satisfied in two ways: (i) by a hexagonal symmetry arising from the right-left doubling of front and back, (ii) along with separate organizations on the two sides that may be required to operate independently to some extent. The eight observed muscle innervation patterns from the data are the complete set of possible combinations of inhibitory/excitatory polarities from three canal pairs. These eight innervation patterns are organized as the vertices of a cube. The two types of side muscles provide the vertical direction. As the head rotates in physical space, the cube rotates in sensorimotor space. Like the canal-neck projection, otolith projections and proprioceptive afferents contact both the vestibular nuclei and neck motoneurons. They may have a similar organization, perhaps with extensions of the same pattern. Otherwise, like a checkerboard superimposed over a paisley, they will form an overlapping organization with the disynaptic canal-neck projection. Further research is required to determine whether the sensorimotor spatial structure of the canal-neck projection is widespread in nervous systems or whether there are several complete structures that are fragmented and reintegrated.     

Experimental research on vestibular compensation using posturography]

Vestibular compensation is a representation of nervous system plasticity which manifests as a gradual recovery of equilibrium function both in vestibulo-spinal system and vestibulo-oculomotor system. In order to assess whether the vestibular compensation is a homogeneous process among the different reflexes, the Authors have studied two groups of subjects affected by peripheral or central lesion. The development of the vestibular compensation has been evaluated by the rotation and posturographic tests. The results demonstrate a constant correlation between rotation and stabilometric parameters in the patients suffering from peripheral dizziness while there isn't any correlation between acceleratory and posturographic tests in patients affected by central vertigo. These results demonstrate that the compensation develops at the different levels of the balance function in a very different and independent way and that comparison of the rotation and posturographic patterns may be useful to establish the peripheral or central site of the lesions.     

Molecular mechanisms of Brainstem plasticity

Vestibular compensation is the process of behavioral recovery that occurs following unilateral deafferentation of the vestibular nerve fibers (unilateral labyrinthectomy, UL). Since UL results in a permanent loss of vestibular input from the ipsilateral vestibular (VIIIth) nerve, vestibular compensation is attributed to CNS plasticity and has been used as a general model of lesion-induced CNS plasticity. Behavioral recovery from the ocular motor and postural symptoms of UL is correlated with a partial return of resting activity to neurons in the vestibular nucleus (VN) on the deafferented side (the "deafferented VN"), and lesions to the deafferented VN prevent compensation; therefore, the regeneration of resting activity within the deafferented VN is believed to have a causal role in vestibular compensation. The biochemical mechanisms responsible for the adaptive neuronal changes within the deafferented VN are poorly understood. Neuropeptide hormone fragments, such as adrenocorticotrophic hormone (ACTH)-4-10, have been shown to accelerate vestibular compensation and can act directly on some VN neurons in vitro. Antagonists for the N-methyl-D-aspartate (NMDA) receptor have been shown to inhibit vestibular compensation if administered early in the compensation process. Biochemical studies in frog indicate marked alterations in the phosphorylation patterns of several proteins during compensation, and the in vitro phosphorylation of some of these proteins is modulated by ACTH-(1-24), calcium (Ca2+), and calmodulin or protein kinase C. It is therefore possible that ACTH fragments and NMDA antagonists (via their effects on NMDA receptor-mediated Ca2+ channels) modulate vestibular compensation through their action on Ca(2+)-dependent pathways within VN neurons. Recent studies have shown that some Ca2+ channel antagonists and the Ca(2+)-dependent enzyme inhibitor calmidazolium chloride facilitate vestibular compensation. How the regulation of Ca2+ may be related to the neuronal changes responsible for vestibular compensation is unclear at present.     

Role of NMDA receptors in the compensation of ocular nystagmus induced by hemilabyrinthectomy in the guinea pig.

The possibility that N-methyl-D-aspartate (NMDA) receptor activation plays a role in inducing the vestibular compensation following hemilabyrinthectomy (HL) in guinea pigs, was verified by means of continuous intraventricular osmotic pumping of DL-2-Amino-5-phosphono-valeric acid (APV). Our results show that high doses (40 and 20 mM) of APV decrease both the combined OKR and VOR and the nystagmus following HL. Low doses of APV (2.5 mM), affect the time course of the ocular compensation by maintaining a higher level of nystagmus beat frequency and by delaying the nystagmus disappearance. On the contrary, the compensation time course is not affected by administering APV later on in the compensation period. Therefore, it appears that NMDA receptors are activated during the precocious phase of vestibular compensation, when a large vestibular imbalance is present. This finding is explained by the development of NMDA receptor hypersensitivity, in the functionally inactivated commissural system or by the occurrence of NMDA-mediated long-term potentiation.     

Model of the effect of the vestibular system on blood pressure during sleep]

A structural model of the effect of vestibular system on blood pressure during sleep is proposed. This model reflects joint action of the otolyth system and semicircular canal system, vestibular nuclei, vasomotor centre, vagus nuclei and of the central control mechanism of the state awakeness -- sleep. Anatomic and physiological prerequisites involved in the model are expressed by chains with transmission functions, signal generators, summators etc.     

Velocity Control of a Bounding Quadruped via Energy Control and Vestibular Reflexes

In this paper a bio-inspired approach of velocity control for a quadruped robot running with a bounding gait on compliant legs is set up. The dynamic properties ofa sagittal plane model of the robot are investigated. By analyzing the stable fixed points based on Poincare map, we find that the energy change of the system is the main source for forward velocity adjustment. Based on the analysis of the dynamics model of the robot, a new simple linear running controller is proposed using the energy control idea, which requires minimal task level feedback and only controls both the leg torque and ending impact angle. On the other hand, the functions of mammalian vestibular reflexes are discussed, and a reflex map between forward velocity and the pitch movement is built through statistical regression analysis. Finally, a velocity controller based on energy control and vestibular reflexes is built, which has the same structure as the mammalian nervous mechanism for body posture control. The new con- troller allows the robot to run autonomously without any other auxiliary equipment and exhibits good speed adjustment capa- bility. A series simulations and experiments were set to show the good movement agility, and the feasibility and validity of the robot system.     

The effect of clinorotation on vestibular compensation in upside-down swimming catfish.

Upside-down swimming catfish Synodontis nigriventris can keep upside-down swimming posture stably under pseudo-microgravity generated by clinostat. When the vestibular organ is unilaterally ablated, the operated S. nigriventris shows disturbed swimming postures under the clinorotation condition. However, about 1 month after the operation, unilateral vestibular organ-ablated S. nigriventris shows stable upside-down swimming posture under the condition (vestibular compensation). In contrast, a closely related upside-up swimming catfish Synodontis multipunctatus belonging to same Synodontis family can not keep stable swimming postures under the clinorotation conditions. In this study, we examined the effect of continuous clinorotation on vestibular compensation in intact and unilateral vestibular organ-ablated Synodontis nigriventris and Synodontis multipunctatus. After the exposure to continuous clinorotation, the postures of the catfish were observed under microgravity provided by parabolic flights of an aircraft. Unilateral vestibular organ-ablated S. nigriventris which had been exposed to continuous clinorotation showed stable swimming postures and did not show dorsal light reaction (DLR) under microgravity. This postural control pattern of the operated catfish was similar to that of intact catfish. Intact and unilateral vestibular organ-ablated S. multipunctatus showed DLR during microgravity. Our results confirmed that S. nigriventris has a novel balance sensation which is not affected by microgravity. DLR seems not to play an important role in postural control. It remains unclear that the continuous clinorotation effects on vestibular compensation because we could not keep used unilateral vestibular organ-ablated fish alive under continuous clinorotation for uninterrupted 25 days. This study suggests that space flight experiments are required to explore whether gravity information is essential for vestibular compensation.     

The development of the static vestibulo-ocular reflex in the Southern Clawed Toad,Xenopus laevis

The static vestibulo-ocular reflex was investigated in tadpoles at different times following unilateral destruction of the labyrinth during the period of early organogenesis and premetamorphosis. Balance compensation is completed after a few weeks, while gain compensation only occurs partially (Figs. 2-4). Tadpoles hemilabyrinthectomized in the age of 2.5 days (stage 38) develop no vestibular nuclei on their lesioned side, while tadpoles operated later in their life, possess these nuclei (Figs. 5, 6) even if they were not detectable at the operation day (Fig. 7). For their dorsal vestibular nucleus (DVN), the number of neurons is usually larger on the intact than on the lesioned side; while for the ventral vestibular nucleus (VVN), there is either numerical symmetry or a transient decrease of cell number on the intact side (Fig. 5). The results demonstrate that vestibular compensation occurs even if vestibular nuclei have developed only on one side, i.e. the vestibular commissure is not a prerequisite for a successful compensation process. It is discussed whether the use of extra-vestibular error signals for balance but not for gain compensation may cause the differences in time courses of both compensation processes.