Smith P F, Darlington C L
Department of Psychology, University of Otago, Dunedin, New Zealand.
Brain Res Brain Res Rev. 1991 May-Aug;16(2):117-33. doi: 10.1016/0165-0173(91)90001-o.
This paper reviews the literature relating to the neurochemical basis of vestibular compensation, a process of behavioral recovery which occurs following the removal of afferent input from one labyrinth (unilateral labyrinthectomy, UL). Although vestibular compensation is known to be correlated with a return of resting activity to the vestibular nucleus (VN) ipsilateral to the UL (the deafferented VN), the neurochemical mechanisms by which this neuronal recovery occurs, are unknown. At present, there is little evidence to support the hypothesis that denervation supersensitivity of excitatory amino acid, dopamine, norepinephrine or acetylcholine receptors in the deafferented VN, is responsible for vestibular compensation: binding studies for glutamate or acetylcholine do not support an upregulation of these receptor types. However, changes in the affinity or efficacy of these receptor complexes cannot be ruled out. There are still many neurotransmitter systems, such as serotonergic and histaminergic systems, which have not been investigated in relation to vestibular compensation. In several species it has been shown that treatment with adrenocorticotropic hormone, fragment 4-10 (ACTH-(4-10], can accelerate vestibular compensation. It is not clear how these drugs exert their effects. In vitro electrophysiological studies have shown that VN neurons are capable of generating resting activity in the absence of their normal afferent inputs and it is possible that these neurons have pacemaker-like membrane characteristics which contribute to the regeneration of activity following UL. Recent biochemical studies have revealed changes in the phosphorylation patterns of a number of proteins during compensation. The possible relationship between these phosphorproteins and the synaptic or membrane changes which are responsible for vestibular compensation remains to be determined.
本文综述了与前庭代偿神经化学基础相关的文献，前庭代偿是一种行为恢复过程，发生在一侧迷路传入输入被切断（单侧迷路切除术，UL）之后。尽管已知前庭代偿与UL同侧前庭核（VN）（去传入VN）静息活动的恢复相关，但这种神经元恢复发生的神经化学机制尚不清楚。目前，几乎没有证据支持去传入VN中兴奋性氨基酸、多巴胺、去甲肾上腺素或乙酰胆碱受体的失神经超敏反应导致前庭代偿这一假说：谷氨酸或乙酰胆碱的结合研究不支持这些受体类型的上调。然而，不能排除这些受体复合物的亲和力或效能发生变化。仍有许多神经递质系统，如血清素能和组胺能系统，尚未针对前庭代偿进行研究。在几个物种中已经表明，用促肾上腺皮质激素片段4 - 10（ACTH - (4 - 10]）治疗可以加速前庭代偿。尚不清楚这些药物是如何发挥作用的。体外电生理研究表明，VN神经元在没有正常传入输入的情况下能够产生静息活动，并且这些神经元可能具有类似起搏器的膜特性，这有助于UL后活动的再生。最近的生化研究揭示了代偿过程中许多蛋白质磷酸化模式的变化。这些磷酸化蛋白与负责前庭代偿的突触或膜变化之间的可能关系仍有待确定。
