Galiana H L, Green A M
Department of Biomedical Engineering, McGill University, Montreal, Quebec, Canada.
Otolaryngol Head Neck Surg. 1998 Sep;119(3):231-43. doi: 10.1016/S0194-5998(98)70058-0.
Vestibular adaptation can be induced optically or by chemical or physical injury to the vestibular apparatus or the brain stem. In searching for the sites or mechanisms of vestibular adaptation, neurophysiologists often rely on comparing central resting (background) activities and central modulations (sensitivity) during vestibular stimulation, before and after motor learning or vestibular compensation. It is assumed that adapted central sites must exhibit modulation changes that parallel vestibulo-ocular reflex changes. Using model simulations and analysis, we will show that such presumptions may be misleading. First, using a simple schematic of interconnected cells or nuclei, one can show that modulation depth and background "tone" can be modified (or fixed) independently, using weightings on direct or indirect afferent projections. That is, if synaptic weights along all stimulus pathways are altered, one may fix or strongly modify central premotor characteristics in a manner apparently unrelated to global reflex changes. In the vestibulo-ocular reflex, the dominant premotor pathways contain position-vestibular-pause cells and eye-head-velocity cells (which are behaviorally similar to floccular-target neurons). Several experiments have reported negligible changes in the velocity sensitivity of position-vestibular-pause cells, despite large gain changes in the vestibulo-ocular reflex induced by training with visual-vestibular conflict. On the other hand, the modulation changes on floccular-target neurons (position-vestibular-pause) can be much larger than the changes in reflex gain. Using a bilateral vestibulo-ocular reflex model, we show that overall increases or decreases in reflex gain can be expressed (even overexpressed) in one particular subgroup of premotor neurons. Nevertheless, such observations are theoretically compatible with synaptic changes on all primary projections in a widely interconnected central network. Hence, stable neural responses during reflex adaptation are not sufficient to exclude a potential site of sensory-motor adaptation. Similarly, modified neural responses (as in cerebellum) need not necessarily imply a direct role in supporting the adapted state. Model predictions should help to design additional experimental protocols, to test hypotheses, and to refine diagnostic measures of recovery after vestibular lesions.
前庭适应可通过光学方法诱导,也可通过对前庭器官或脑干进行化学或物理损伤来诱导。在寻找前庭适应的部位或机制时,神经生理学家通常依靠比较运动学习或前庭代偿前后,前庭刺激期间的中枢静息(背景)活动和中枢调制(敏感性)。人们认为,适应的中枢部位必须表现出与前庭眼反射变化平行的调制变化。通过模型模拟和分析,我们将表明这种假设可能会产生误导。首先,使用相互连接的细胞或核的简单示意图,可以表明调制深度和背景“音调”可以通过对直接或间接传入投射的加权独立地修改(或固定)。也就是说,如果沿所有刺激途径的突触权重发生改变,人们可能会以一种明显与整体反射变化无关的方式固定或强烈修改中枢运动前特征。在前庭眼反射中,主要的运动前通路包含位置-前庭-暂停细胞和眼-头速度细胞(其行为与绒球目标神经元相似)。几项实验报告称,尽管通过视觉-前庭冲突训练诱导前庭眼反射的增益发生了很大变化,但位置-前庭-暂停细胞的速度敏感性变化可忽略不计。另一方面,绒球目标神经元(位置-前庭-暂停)的调制变化可能比反射增益的变化大得多。使用双侧前庭眼反射模型,我们表明反射增益的总体增加或减少可以在一个特定的运动前神经元亚组中表达(甚至过度表达)。然而,从理论上讲,这些观察结果与广泛互连的中枢网络中所有主要投射上的突触变化是兼容的。因此,反射适应期间稳定的神经反应不足以排除感觉运动适应的潜在部位。同样,修改后的神经反应(如在小脑中)不一定意味着在支持适应状态方面有直接作用。模型预测应有助于设计额外的实验方案,以检验假设,并完善前庭病变后恢复的诊断措施。