首页> 美国卫生研究院文献>The Journal of Physiology >Differential effect of injections of kainic acid into the prepositus and the vestibular nuclei of the cat.
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Differential effect of injections of kainic acid into the prepositus and the vestibular nuclei of the cat.

机译:向猫的垂体和前庭核中注入海藻酸的效果不同。

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摘要

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)
机译:1.为了充分控制眼睛的运动,必须同时向眼动神经元提供眼速度信号和眼位信号。但是,动眼系统的所有命令信号都是速度信号。如今,关于脑干网络的存在已达成普遍共识,该脑干网络会将速度命令信号转换为眼位信号。由于其功能,该电路称为动眼神经积分器。最终失败的最明显症状是保持视线的缺陷:在这种情况下,扫视之后是向心后跳音。尽管动眼神经积分器是动眼运动理论的中心,但其确切位置仍是一个有争议的问题。 2.以前,发现在猫和猴中微量注射海藻酸(KA)到垂体前核(NPH)和前庭内侧核(MVN)区域均引起水平凝视失败。然而,这些注射中使用的相对较大的体积(1-3微升)和浓度(2-4微克微升-1)使得很难知道观察到的缺陷是由于NPH还是附近的MVN的干扰。这些考虑导致我们向猫的NPN的鼻端或沿猫的NPH的不同部位注入了非常少量的海藻酸(50 nl,0.1微克微升-1)。 3.使用搜索线圈技术记录(1)自发眼动(2)恒速旋转(50度s-1持续40 s)和视动性眼球震颤(OKN)诱发的前庭眼反射(VOR) )是通过在30度s-1旋转视动鼓40 s引起的。 4.在每个注射实验中,通过记录外展神经受刺激诱发的反领域磁场电位,绘制出警觉猫外展核的位置。然后将两个微量移液器粘合在一起,以使当记录微量移液器的尖端位于外展核的中心时,注射微量移液器的尖端位于目标区域。然后将双移液管降低到脑干中,直到记录的微移液管到达外展核的中心。然后通过气压系统通过注射微量移液管将海藻酸注射到警觉猫的脑干中。 5.按照这样的方案进行,向NPH或MVN的喙部注射KA始终导致特定的眼动变化。(摘要截断为400字)

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