Saccade-related inhibitory input to pontine omnipause neurons: An intracellular study in alert cats
Saccade-related inhibitory input to pontine omnipause neurons: An intracellular study in alert cats
复制标题
DOI：
10.1152/jn.1999.82.3.1198
复制
发表时间：
1999-09-01
影响因子：
2.5
通讯作者：
Shimazu, H
中科院分区：
文献类型：
--
作者：
Yoshida, K;Iwamoto, Y;Shimazu, H
全暂停神经元（Omnipause neurons，OPN）是脑桥中线神经元，被认为控制许多眼球运动行为，特别是扫视。细胞内记录从OPN在警觉猫阐明扫视相关的突触后事件的OPNs，从而确定什么样的传入放电模式冲击OPN，导致他们的扫视抑制。在每次扫视之前，穿刺的OPN的膜电位表现出陡峭的超极化，并持续整个扫视期间。细胞内注入Cl-可使超极化逆转为去极化，表明其由抑制性突触后电位（IPSPs）的时间总和组成。扫视相关的超极化的持续时间几乎等于同时扫视的持续时间。超极化的时间过程与桡眼速度的时间过程相似，除了初始阶段。在眼速下降期，超极化瞬时振幅与眼速瞬时值之间存在高度显著的相关性。眼速度峰值处的超极化幅度与眼速度峰值显著相关。超极化的时间积分与眼跳的径向幅度相关。超极化和眼速之间的初始相位差是由于初始陡峭超极化的峰值时间（类似于20 ms）的相对恒定性，而不管与眼速共变的后期电位曲线如何。最初的陡峭超极化导致扫视开始15.9 +/- 3.8（SD）ms，这比中等-不良爆发神经元的时间长。这些结果表明，暂停的活动在OPNs是由IPSPs发起的突然，强烈的输入和维护，为整个持续时间的扫视，由传入传递眼速度信号。我们认为，最初的突然抑制起源于中央结构，如上级丘和额叶眼场和眼速度相关的抑制起源于突发发生器在脑干。
Omnipause neurons (OPNs) are midline pontine neurons that are thought to control a number of oculomotor behaviors, especially saccades. Intracellular recordings were made from OPNs in alert cats to elucidate saccade-associated postsynaptic events in OPNs and thereby determine what patterns of afferent discharge impinge on OPNs to cause their saccadic inhibition. The membrane potential of impaled OPNs exhibited steep hyperpolarization before each saccade that lasted for the whole period of the saccade. The hyperpolarization was reversed to depolarization by intracellular injection of Cl- ions, indicating it consisted of temporal summation of inhibitory postsynaptic potentials (IPSPs). The duration of the saccade-related hyperpolarization was almost equal to the duration of the concurrent saccades. The time course of the hyperpolarization was similar to that of the radial eye velocity except for the initial phase. During the falling phase of eye velocity, the correlation between the instantaneous amplitude of hyperpolarization and the instantaneous eye velocity was highly significant. The amplitude of hyperpolarization at the eye velocity peak was correlated significantly with the peak eye velocity. The time integral of the hyperpolarization was correlated with the radial amplitude of saccades. The Initial phase disparity between the hyperpolarization and eye velocity was due to the relative constancy of peak time (similar to 20 ms) of the initial steep hyperpolarization regardless of the later potential profile that covaried with the eye velocity. The initial steep hyperpolarization led the beginning of saccades by 15.9 +/- 3.8 (SD) ms, which is longer than the lend time for medium-bad burst neurons. These results demonstrate that the pause of activity in OPNs is caused by IPSPs initiated by an abrupt, intense input and maintained, for the whole duration of the saccade, by afferents conveying eye velocity signals. We suggest that the initial sudden inhibition originates from central structures such as the superior colliculus and frontal eye fields and that the eye velocity-related inhibition originates fi om the burst generator in the brain stem.