Darlington C L, Smith P F
Department of Psychology, University of Otago, Dunedin, New Zealand.
J Vestib Res. 1996 May-Jun;6(3):185-201.
This theoretical paper describes the "intrinsic mechanism hypothesis," a new hypothesis of vestibular compensation, the behavioral recovery that follows unilateral deafferentation of the vestibular labyrinth (UVD). The most salient characteristic of vestibular compensation is the decrease in the severity of the static ocular motor and postural symptoms that follow UVD, associated with a recovery of resting activity in the ipsilateral vestibular nucleus complex (VNC). The speed of static compensation in some mammalian species (for example, cat) has suggested that reactive synaptogenesis is an unlikely explanation because it is too slow. Other, more rapid mechanisms, such as denervation supersensitivity, receptor-up-regulation, or increased neurotransmitter release, were reasonable possibilities. However, to date, each study that has addressed these possibilities has failed to find any change that could account for the recovery of VNC resting activity. The search for such "substitutive" mechanisms was based on the hypothesis that something other than the VNC neurons themselves would have to "replace" the missing resting activity that the ipsilateral vestibular nerve normally provides. However, brainstem slice studies demonstrate that, at least in vitro, VNC neurons do not need the vestibular nerve in order to generate resting activity. On the basis of these and other considerations, we suggest that following a brief calcium-induced diaschisis, VNC neurons ipsilateral to the UVD reactivate the intrinsic membrane properties that normally contribute to their resting activity in vivo, and that this recovery of resting activity accounts for static vestibular compensation.
这篇理论性论文描述了“内在机制假说”，这是一种关于前庭代偿的新假说，即前庭迷路单侧传入神经阻滞（UVD）后出现的行为恢复。前庭代偿最显著的特征是UVD后静态眼动和姿势症状的严重程度降低，同时同侧前庭核复合体（VNC）的静息活动恢复。一些哺乳动物物种（如猫）的静态代偿速度表明，反应性突触形成不太可能是原因，因为它太慢了。其他更快的机制，如去神经超敏反应、受体上调或神经递质释放增加，是合理的可能性。然而，迄今为止，每项探讨这些可能性的研究都未能发现任何能够解释VNC静息活动恢复的变化。对这种“替代性”机制的探索基于这样一种假设，即除了VNC神经元本身之外，必须有其他东西来“替代”同侧前庭神经通常提供的缺失的静息活动。然而，脑干切片研究表明，至少在体外，VNC神经元产生静息活动并不需要前庭神经。基于这些及其他考虑因素，我们认为，在短暂的钙诱导神经功能联系障碍之后，UVD同侧的VNC神经元重新激活了通常在体内有助于其静息活动的内在膜特性，并且这种静息活动的恢复解释了静态前庭代偿。
