Ryan L J, Clark K B
Department of Psychology, Oregon State University, Corvallis 97331-5303.
Exp Brain Res. 1991;86(3):641-51. doi: 10.1007/BF00230538.
We investigated how the cerebral cortex can influence the globus pallidus by two routes: the larger, net inhibitory route through the neostriatum and the separate, smaller, net excitatory route through the subthalamic nucleus. Stimulation (0.3 and 0.7 mA) of two regions of frontal agranular (motor) cortex and of the medial orbitofrontal cortex centered in the prelimbic cortex typically elicited one or more of the following extracellularly recorded responses in over 50% of tested cells: an initial excitation (approximately 6 ms latency), a short inhibition (15 ms latency) and a late excitation (29 ms latency). Some other cells responded with an excitatory response only (18 ms latency). The excitatory responses largely arise from the subthalamic route. Kainic acid or electrolytic lesion of the subthalamic nucleus eliminated most excitatory responses and greatly prolonged the duration (16 vs 50 ms) of the inhibition. Subthalamic neurons typically showed one or more of the following responses to cortical stimulation: an early excitatory response (4 ms latency), an inhibitory period (9 ms) and a late excitatory response (16 ms). The early response was seen after motor cortex but not prelimbic stimulation. The timing of the globus pallidus and subthalamic responses suggest the operation of a reciprocal inhibitory/excitatory pathway. Two reciprocal interactions were indicated. First, pallidal inhibition may disinhibit the subthalamus and, via a feedback pathway onto the same pallidal cells, act to terminate the neostriatal-induced inhibition. Second, there may be a feedforward pathway from pallidal cells to subthalamic neurons to a different group of pallidal cells. This pathway could act to suppress competing responses. Thus the subthalamus may have three actions: 1) an early direct cortical and 2,3) later reciprocal feedforward and feedback excitatory antagonism of the neostriatal mediated inhibition of globus pallidus.
一条是通过新纹状体的较大的净抑制性途径，另一条是通过底丘脑核的独立的较小的净兴奋性途径。刺激额叶无颗粒（运动）皮层的两个区域以及以边缘前皮层为中心的内侧眶额皮层（刺激强度为0.3和0.7毫安），通常在超过50%的受试细胞中会在细胞外记录到以下一种或多种反应：初始兴奋（潜伏期约6毫秒）、短暂抑制（潜伏期15毫秒）和晚期兴奋（潜伏期29毫秒）。其他一些细胞仅表现出兴奋性反应（潜伏期18毫秒）。兴奋性反应主要源于底丘脑途径。用 kainic 酸或电解损毁底丘脑核可消除大多数兴奋性反应，并大大延长抑制的持续时间（从16毫秒延长至50毫秒）。底丘脑神经元对皮层刺激通常表现出以下一种或多种反应：早期兴奋性反应（潜伏期4毫秒）、抑制期（9毫秒）和晚期兴奋性反应（潜伏期16毫秒）。运动皮层刺激后可观察到早期反应，但边缘前皮层刺激后未观察到。苍白球和底丘脑反应的时间表明存在一种相互抑制/兴奋途径。表明存在两种相互作用。首先，苍白球抑制可能解除对底丘脑的抑制，并通过反馈途径作用于相同的苍白球细胞，从而终止新纹状体诱导的抑制。其次，可能存在一条从苍白球细胞到底丘脑神经元再到另一组苍白球细胞的前馈途径。该途径可起到抑制竞争反应的作用。因此，底丘脑可能具有三种作用：1）早期直接接受皮层输入，2）后期对新纹状体介导的苍白球抑制进行相互前馈和反馈兴奋性拮抗。
