Saccade-related inputs to the saccade generator : an intracellular study in alert cats

眼球运动神经元(OPN)是脑桥中线神经元，被认为控制着许多眼球运动行为，特别是眼跳。在警觉猫的OPN上进行细胞内记录，以阐明与眼跳相关的突触后事件，从而确定什么传入放电模式冲击到ONs，从而导致其眼跳抑制。OPN的膜电位在每次扫视前呈现陡峭的超极化，并持续到整个扫视周期。细胞内注入C1-离子后，超极化被逆转为去极化，表明它由抑制性突触后电位(IPSP)组成。超极化的持续时间几乎等于眼跳的持续时间。除初始时相外，超极化的时程与径向眼速的时程相似。在眼速下降阶段，超极化瞬时幅度与瞬时…之间的相关性眼球运动速度越快，差异非常显著。眼速峰值处的超极化幅度与眼速峰值显著相关。超极化的时间积分与眼跳的幅度相关。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相对恒定所致，而与随眼速变化的后期电位分布无关。超极化导致眼跳开始的时间为16ms，比中速爆发式神经元的前导时间要长。这些结果表明，OPNS的活动暂停是由突然、强烈的输入引起的LPSP引起的，而在整个眼跳过程中，LPSP是由传递眼速信号的传入所引起的。我们认为，最初的突发性抑制起源于上丘等中枢结构，而眼速相关的抑制起源于脑干的猝发发生器。较少

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 and thereby determine what patterns of afferent discharge impinge upon OPNs to cause their saccadic inhibition. The membrane potential of OPNs exhibited steep hyperpolarization before each saccade which lasted for the whole period of the saccade. The hyperpolarization was reversed to depolarization by intracellular injection of C1- ions, indicating it consisted of inhibitory postsynaptic potentials (IPSPs). The duration of the hyperpolarization was almost equal to the duration of the 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 … More eye velocity was highly significant. The amplitude of hyperpolarization at the eye velocity peak was significantly correlated with the peak eye velocity. The time integral of the hyperpolarization was correlated with the amplitude of saccades. The initial phase disparity between the hyperpolarization and eye velocity was due to the relative constancy of peak time of the initial steep hyperpolarization regardless of the later potential profile that covaried with the eye velocity. The hyperpolarization led the beginning of saccades by 16 ms, which is longer than the lead time for medium-lesd burst neurons. These results demonstrate that the pause of activity in OPNs is caused by LPSPs initiated by an abrupt, intense input and maintained, for the whole duration of saccade, by afferents conveying eye velocity signals. We suggest that the initial sudden inhibition originates from central structures such as the superior colliculus and that the eye velocity-related inhibition originates from the burst generator in the brain stem. Less