Smooth-pursuit eye-movement deficits with chemical lesions in macaque nucleus reticularis tegmenti pontis.

Smooth-pursuit eye-movement deficits with chemical lesions in macaque nucleus reticularis tegmenti pontis.
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猕猴脑桥网状核化学损伤导致平滑追踪眼球运动缺陷。

DOI:
10.1152/jn.1999.82.3.1178
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发表时间:
1999
期刊:
Journal of neurophysiology.
影响因子:
--
通讯作者:
Yee,RD
Yee,RD
中科院分区:
--
文献类型:
--
作者:
Suzuki,DA;Yamada,T;Hoedema,R;Yee,RD

文献摘要

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解剖和神经元记录表明,猕猴被盖网状脑桥核(NRTP)可能是皮质-桥脑-小脑通路的主要脑桥成分,有助于控制平稳追踪的眼球运动。这种通路的存在与双侧桥背外侧核损伤后缺乏永久性追踪性损害有关。为了提供更直接的证据证明NRTP参与调节顺畅的眼球运动,对猕猴NRTP进行了化学损伤,方法是注射利多卡因或鹅膏油酸。首先通过记录神经元活动中与平滑追踪相关的调制来识别注射部位。由此产生的损害在维持和启动顺畅追逐眼球运动方面都造成了显著的缺陷。病变形成后,恒速、保持平稳追踪眼球运动的增益平均下降44%。保持顺畅追赶眼球运动的能力在∼3天后恢复,当保持的追赶收益达到正常值时。采用阶梯式“Rashbass”任务,考察病变对平滑追踪眼球运动启动的影响。在开始追踪的最初80毫秒内的平均眼球加速被测定,并发现在给予鹅膏糖酸后,平均减少了48%。顺畅追逐眼球运动的启动和维持的损害本质上是方向性的。向上追逐似乎是最脆弱的,在所有情况下都受到损害,与所调查的损害因素和追逐类型无关。在NRTP中,向下平滑追求似乎更能抵抗化学损伤的影响。以同侧和对侧定向追踪的缺陷为例,观察到水平追踪的缺陷。这一结果为基于生理和解剖学的结论提供了行为学支持,即NRTP是皮质-桥脑-小脑回路的组成部分,可能涉及额叶眼场(FEF)的追踪区,并投射到小脑的眼运动相关区域。这条FEF-NRTP-小脑通路将平行于大脑中、内侧颞上皮质区-桥背外侧核-小脑通路,该通路也参与调节顺行追踪眼球运动。
Anatomic and neuronal recordings suggest that the nucleus reticularis tegmenti pontis (NRTP) of macaques may be a major pontine component of a cortico-ponto-cerebellar pathway that subserves the control of smooth-pursuit eye movements. The existence of such a pathway was implicated by the lack of permanent pursuit impairment after bilateral lesions in the dorsolateral pontine nucleus. To provide more direct evidence that NRTP is involved with regulating smooth-pursuit eye movements, chemical lesions were made in macaque NRTP by injecting either lidocaine or ibotenic acid. Injection sites first were identified by the recording of smooth-pursuit-related modulations in neuronal activity. The resulting lesions caused significant deficits in both the maintenance and the initiation of smooth-pursuit eye movements. After lesion formation, the gain of constant-velocity, maintained smooth-pursuit eye movements decreased, on the average, by 44%. Recovery of the ability to maintain smooth-pursuit eye movements occurred over ∼3 days when maintained pursuit gains attained normal values. The step-ramp, “Rashbass” task was used to investigate the effects of the lesions on the initiation of smooth-pursuit eye movements. Eye accelerations averaged over the initial 80 ms of pursuit initiation were determined and found to be decremented, on the average, by 48% after the administration of ibotenic acid. Impairments in the initiation and maintenance of smooth-pursuit eye movements were directional in nature. Upward pursuit seemed to be the most vulnerable and was impaired in all cases independent of lesioning agent and type of pursuit investigated. Downward smooth pursuit seemed more resistant to the effects of chemical lesions in NRTP. Impairments in horizontal tracking were observed with examples of deficits in ipsilaterally and contralaterally directed pursuit. The results provide behavioral support for the physiologically and anatomic-based conclusion that NRTP is a component of a cortico-ponto-cerebellar circuit that presumably involves the pursuit area of the frontal eye field (FEF) and projects to ocular motor-related areas of the cerebellum. This FEF-NRTP-cerebellum path would parallel a middle and medial superior temporal cerebral cortical area-dorsolateral pontine nucleus-cerebellum pathway also known to be involved with regulating smooth-pursuit eye movements.