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向猫的前庭前置核和前庭核注射海藻酸的差异效应。

Differential effect of injections of kainic acid into the prepositus and the vestibular nuclei of the cat.

作者信息

Godaux E, Mettens P, Cheron G

机构信息

Laboratory of Neurophysiology, University of Mons-Hainaut, Faculty of Medicine, Belgium.

出版信息

J Physiol. 1993 Dec;472:459-82. doi: 10.1113/jphysiol.1993.sp019956.

Abstract
  1. In order adequately to control eye movements, oculomotoneurones have to be supplied with both an eye-velocity signal and an eye-position signal. However, all the command signals of the oculomotor system are velocity signals. Nowadays, there is general agreement about the existence of a brainstem network that would convert velocity command-signals into an eye-position signal. This circuit, because of its function, is called the oculomotor neural integrator. The most obvious symptom of its eventual failure is a gaze-holding deficit: in this case, saccades are followed by a centripetal post-saccadic drift. Although the oculomotor neural integrator is central in oculomotor theory, its precise location is still a matter for debate. 2. Previously, microinjections of kainic acid (KA) into the region of the nucleus prepositus hypoglossi (NPH) and of the medial vestibular nucleus (MVN) were found to induce a horizontal gaze-holding failure both in the cat and in the monkey. However, the relatively large volumes (1-3 microliters) and concentrations (2-4 micrograms microliters-1) used in these injections made it difficult to know if the observed deficit was due to a disturbance of the NPH or of the nearby MVN. These considerations led us to inject very small amounts of kainic acid (50 nl, 0.1 microgram microliter-1) either into the rostral part of the MVN or into different sites along the NPH of the cat. 3. The search coil technique was used to record (1) spontaneous eye movements (2) the vestibulo-ocular reflex (VOR) induced by a constant-velocity rotation (50 deg s-1 for 40 s) and the optokinetic nystagmus (OKN) elicited by rotating an optokinetic drum at 30 deg s-1 for 40 s. 4. In each injection experiment, the location of the abducens nucleus of the alert cat was mapped out by recording the antidromic field potentials evoked by the stimulation of the abducens nerve. Two micropipettes were then glued together in such a way that when the tip of the recording micropipette was in the centre of the abducens nucleus the tip of the injection micropipette was in a target area. The twin pipettes were then lowered in the brainstem until the recording micropipette reached the centre of the abducens nucleus. Kainic acid was then injected into the brainstem of the alert cat through the injection micropipette by an air pressure system. 5. Carried out according to such a protocol, KA injections into the NPH or the rostral part of the MVN consistently led to specific eye-movement changes.(ABSTRACT TRUNCATED AT 400 WORDS)
摘要
  1. 为了充分控制眼球运动,眼球运动神经元必须同时接收眼球速度信号和眼球位置信号。然而,眼球运动系统的所有指令信号都是速度信号。如今,人们普遍认为存在一个脑干网络,它能将速度指令信号转换为眼球位置信号。由于其功能,这个回路被称为眼球运动神经整合器。其最终故障最明显的症状是凝视保持缺陷:在这种情况下,扫视之后会出现向心性扫视后漂移。尽管眼球运动神经整合器在眼球运动理论中至关重要,但其确切位置仍存在争议。2. 此前,人们发现向舌下前置核(NPH)区域和内侧前庭核(MVN)微量注射 kainic 酸(KA)会在猫和猴子身上诱发水平凝视保持失败。然而,这些注射中使用的相对较大体积(1 - 3 微升)和浓度(2 - 4 微克/微升)使得难以确定观察到的缺陷是由于 NPH 还是附近的 MVN 受到干扰。这些考虑因素促使我们向猫的 MVN 头部或沿 NPH 的不同部位注射极少量的 kainic 酸(50 纳升,0.1 微克/微升)。3. 使用搜索线圈技术记录(1)自发眼球运动(2)由恒速旋转(50 度/秒,持续 40 秒)诱发的前庭眼反射(VOR)以及由以 30 度/秒旋转视动鼓持续 40 秒诱发的视动性眼球震颤(OKN)。4. 在每次注射实验中,通过记录外展神经刺激诱发的逆向场电位来确定清醒猫外展核的位置。然后将两个微吸管粘在一起,使得当记录微吸管的尖端位于外展核中心时,注射微吸管的尖端位于目标区域。然后将双管吸管放入脑干,直到记录微吸管到达外展核中心。然后通过气压系统通过注射微吸管将 kainic 酸注入清醒猫的脑干。5. 按照这样的方案进行操作,向 NPH 或 MVN 头部注射 KA 始终会导致特定的眼球运动变化。(摘要截断于 400 字)
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d20/1160496/ea5f5841ab32/jphysiol00414-0461-a.jpg

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