Effect of cerebellar inactivation by lidocaine microdialysis on the vestibuloocular reflex in goldfish.
Effect of cerebellar inactivation by lidocaine microdialysis on the vestibuloocular reflex in goldfish.
复制标题
利多卡因微透析失活小脑对金鱼前庭眼反射的影响。
DOI：
10.1152/jn.1998.79.3.1286
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Polk,J
中科院分区：
文献类型：
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作者：
McElligott,JG;Beeton,P;Polk,J
McElligott，J. G.，Phyllis Beeton和Jeffrey Polk。利多卡因微透析对金鱼前庭眼反射的小脑失活作用。神经生理学杂志。79：1286-1294，1998。本研究以金鱼为实验动物，通过局部微透析或注射利多卡因，观察前庭小脑失活过程中前庭眼反射的表现和适应性。在光中，在正弦偏航旋转（1/8 Hz ± 20°）期间，眼球速度完全补偿了头部速度（Vis-VOR）。在黑暗中，反射（VOR）增益略有降低（增益为0.8-0.9）。在Vis-VOR和VOR中，在前庭小脑中的利多卡因微透析1小时后，增益都没有改变。在适应反射增益之前，由同相或异相视觉前庭刺激产生的Vis-VOR反射增益的初始抑制或增强也不受小脑失活的影响。随后，在人工脑脊液（CSF）微透析过程中，以同相或反相模式（采集相）进行3 h的适应性反射训练，分别降低（0.30 ± 0.09）和增加（1.60 ± 0.08）VOR增益。然而，利多卡因的微透析完全阻断自适应增益的变化，在3-4小时的连续应用期间。这种影响是可逆的，因为VOR增益变化是在利多卡因被CSF替代作为透析液后1小时产生的。在适应性训练后，在黑暗中的3小时内（保持期），双侧前庭小脑注射CSF（0.25 μl/侧）并没有改变适应性增益变化的正常保持或衰减。然而，注射利多卡因到前庭小脑完全阻止保留的适应VOR增益返回到适应前记录的值。与急性或慢性手术切除相反，通过微透析对小脑进行利多卡因灭活，在增益范围从0.3至1.4的宽范围内，不会改变Vis-VOR和VOR行为或交互式Vis-VOR性能。因此，短期VOR运动学习是一个动态的过程，需要脑干小脑回路的连续操作，或者小脑内或直接受小脑影响的可修改的位点。我们的数据支持后一种假设，因为直接脑干VOR通路似乎是不变的小脑失活后，因此，独立的VOR适应状态。
McElligott, J. G., Phyllis Beeton, and Jeffrey Polk.Effect of cerebellar inactivation by lidocaine microdialysis on the vestibuloocular reflex in goldfish.J. Neurophysiol.79: 1286–1294, 1998. Vestibuloocular reflex performance and adaptation were examined during vestibulocerebellar inactivation by localized lidocaine microdialysis or injection in goldfish. In the light, eye velocity perfectly compensated for head velocity (Vis-VOR) during sinusoidal yaw rotation (1/8 Hz ± 20°). In the dark, the reflex (VOR) gain was slightly reduced (gain ≈ 0.8–0.9). In neither Vis-VOR nor VOR, was gain altered after 1 h of lidocaine microdialysis in the vestibulocerebellum. Before adaptation of reflex gain, the initial suppression or augmentation of Vis-VOR reflex gain produced by in-phase or out-of-phase visual-vestibular stimulation was also unaffected by cerebellar inactivation. Subsequently, 3 h of adaptive reflex training in either the in-phase or out-of-phase paradigm (acquisition phase) respectively decreased (0.30 ± 0.09) or increased (1.60 ± 0.08) VOR gain during artificial cerebral spinal fluid (CSF) microdialysis. However, microdialysis of lidocaine completely blocked adaptive gain changes during a 3–4 h period of continuous application. This effect was reversible because VOR gain changes were produced 1 h after lidocaine was replaced with CSF as the dialysate. After adaptive training, bilateral CSF injections (0.25 μl/side) into the vestibulocerebellum did not alter the normal retention or decay of adapted gain changes during a 3 h period in the dark (retention phase). However, injection of lidocaine into the vestibulocerebellum completely blocked retention of the adapted VOR gain returning the gain to values recorded before adaptation. In contrast to either acute or chronic surgical removal, lidocaine inactivation of the cerebellum by microdialysis did not alter either Vis-VOR and VOR behavior or interactive Vis-VOR performance over a wide range of gain extending from 0.3 to 1.4. Thus short-term VOR motor learning is a dynamic process requiring either continuous operation of brain stem cerebellar loops or, alternatively, modifiable sites within or directly influenced by the cerebellum. Our data supports the latter hypothesis, because the direct brain stem VOR pathways appear to be unaltered after cerebellar inactivation, and, hence, independent of the VOR-adapted state.