Delgado-García José M, Yajeya Javier, Navarro-López Juan de Dios
División de Neurociencias, Universidad Pablo de Olavide, 41013-Seville, Spain.
Prog Brain Res. 2006;154:211-24. doi: 10.1016/S0079-6123(06)54011-7.
It is generally accepted that the prepositus hypoglossi (PH) nucleus is the site where horizontal eye-velocity signals are integrated into eye-position ones. However, how does this neural structure produce the sustained activity necessary for eye fixation? The generation of the neural activity responsible for eye-position signals has been studied here using both in vivo and in vitro preparations. Rat sagittal brainstem slices including the PH nucleus and the paramedian pontine reticular formation (PPRF) rostral to the abducens nucleus were used for recording intracellularly the synaptic activation of PH neurons from the PPRF. Single electrical pulses applied to the PPRF showed a monosynaptic projection on PH neurons. This synapse was found to be glutamatergic in nature, acting on alpha-amino-3-hydroxy-5-methylisoxazole propionate (AMPA)/kainate receptors. Train stimulation (100 ms, 50-200 Hz) of the PPRF evoked a depolarization of PH neurons, exceeding (by hundreds of ms) the duration of the stimulus. Both duration and amplitude of this long-lasting depolarization were linearly related to train frequency. The train-evoked sustained depolarization was demonstrated to be the result of the additional activation of cholinergic fibers projecting onto PH neurons, because it was prevented by slice superfusion with atropine sulfate and pirenzepine (two cholinergic antagonists), and mimicked by carbachol and McN-A-343 (two cholinergic agonists). These results were confirmed in alert behaving cats. Microinjections of atropine and pirenzepine evoked an ipsilateral gaze-holding deficit consisting of an exponential-like, centripetal eye movement following saccades directed toward the injected site. These findings suggest that the sustained activity present in PH neurons carrying eye-position signals is the result of the combined action of PPRF neurons and the facilitative role of cholinergic terminals, both impinging on PH neurons. The present results are discussed in relation to other proposals regarding integrative properties of PH neurons and/or related neural circuits.
一般认为，舌下前置核（PH）是水平眼速信号整合为眼位信号的部位。然而，这种神经结构是如何产生眼球注视所需的持续活动的呢？本文利用体内和体外实验制剂研究了负责眼位信号的神经活动的产生。包含PH核以及展神经核前方的脑桥旁正中网状结构（PPRF）的大鼠矢状脑干切片用于细胞内记录来自PPRF的PH神经元的突触激活。施加于PPRF的单个电脉冲在PH神经元上显示出单突触投射。发现这种突触本质上是谷氨酸能的，作用于α-氨基-3-羟基-5-甲基异恶唑丙酸（AMPA）/海人藻酸受体。对PPRF进行串刺激（100毫秒，50 - 200赫兹）可诱发PH神经元去极化，其持续时间超过（数百毫秒）刺激持续时间。这种长时去极化的持续时间和幅度均与串刺激频率呈线性相关。串刺激诱发的持续去极化被证明是投射到PH神经元上的胆碱能纤维额外激活的结果，因为用硫酸阿托品和哌仑西平（两种胆碱能拮抗剂）对切片进行灌流可阻止其发生，而卡巴胆碱和 McN - A - 343（两种胆碱能激动剂）可模拟其发生。这些结果在清醒行为猫中得到了证实。微量注射阿托品和哌仑西平会诱发同侧凝视保持缺陷，表现为在朝注射部位的扫视后出现指数样向心性眼球运动。这些发现表明，携带眼位信号的PH神经元中存在的持续活动是PPRF神经元的联合作用以及胆碱能终末的促进作用共同作用于PH神经元的结果。本文结果与关于PH神经元和/或相关神经回路整合特性的其他观点进行了讨论。
