Darlington C L, Flohr H, Smith P F
Department of Psychology, University of Otago, Dunedin, New Zealand.
Mol Neurobiol. 1991;5(2-4):355-68. doi: 10.1007/BF02935558.
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.
前庭代偿是指在前庭神经纤维单侧传入阻滞（单侧迷路切除术，UL）后发生的行为恢复过程。由于UL导致同侧前庭（第八）神经的前庭输入永久性丧失，前庭代偿归因于中枢神经系统可塑性，并已被用作损伤诱导的中枢神经系统可塑性的一般模型。从UL的眼球运动和姿势症状中恢复的行为与去传入侧前庭核（VN）中神经元静息活动的部分恢复相关（“去传入VN”），而去传入VN的损伤会阻止代偿；因此，去传入VN内静息活动的恢复被认为在前庭代偿中起因果作用。对去传入VN内适应性神经元变化的生化机制了解甚少。神经肽激素片段，如促肾上腺皮质激素（ACTH）-4-10，已被证明可加速前庭代偿，并可在体外直接作用于一些VN神经元。N-甲基-D-天冬氨酸（NMDA）受体拮抗剂已被证明，如果在代偿过程早期给药，可抑制前庭代偿。青蛙的生化研究表明，在代偿过程中几种蛋白质的磷酸化模式有明显改变，其中一些蛋白质的体外磷酸化受ACTH-（1-24）、钙（Ca2+）、钙调蛋白或蛋白激酶C调节。因此，ACTH片段和NMDA拮抗剂（通过它们对NMDA受体介导的Ca2+通道的作用）可能通过作用于VN神经元内的Ca（2+）依赖性途径来调节前庭代偿。最近的研究表明，一些Ca2+通道拮抗剂和Ca（2+）依赖性酶抑制剂氯氮草可促进前庭代偿。目前尚不清楚Ca2+的调节与负责前庭代偿的神经元变化之间的关系。
