Chung J M, Fang Z R, Hori Y, Lee K H, Willis W D
Marine Biomedical Institute, Departments of Anatomy and Physiology and Biophysics, University of Texas Medical Branch, Galveston, TX 77550-2772 U.S.A.
Pain. 1984 Jul;19(3):259-275. doi: 10.1016/0304-3959(84)90004-6.
Inhibition of spinothalamic tract (STT) cells was produced by repetitive peripheral nerve conditioning stimulation with high intensity and low frequency pulses. Identified STT cells were recorded from the lumbosacral spinal cord of intact, anesthetized monkeys. In addition, presumed STT cells were recorded from both unanesthetized, decerebrated and decerebrated, spinalized monkeys. These cells were identified by antidromically activating them from the contralateral ventral lateral funiculus of the cervical spinal cord. Both C fiber activity evoked by electrical stimulation of the sural nerve and activity evoked by noxious heat were greatly inhibited by repetitive conditioning stimuli applied either to the common peroneal or tibial nerve with a strong enough intensity for activation of C fibers at 2 Hz for 15 min. The inhibition was maintained during the period of conditioning stimulation and often outlasted stimulation by 20-30 min. The inhibition of cells produced by peripheral nerve stimulation was observed in decerebrate and spinalized animals as well as in intact anesthetized monkeys, although the mean recovery time in the decerebrate group was faster. This indicates that anesthetics did not interfere with the inhibitory mechanism. Furthermore, the presence of inhibition in spinalized animals means the inhibition must depend in part on spinal cord neuronal circuitry. Intravenous injection of naloxone produced a significant but small reduction of the recovery phase of the inhibition. No pharmacological agent was found that substantially interfered with the powerful inhibition produced during peripheral conditioning stimuli. The experimental animal model used in these experiments seems appropriate for studying the mechanisms of analgesia produced by peripheral nerve stimulation.
通过高强度低频脉冲对周围神经进行重复性条件刺激可产生脊髓丘脑束（STT）细胞的抑制。在完整、麻醉的猴子的腰骶脊髓中记录已鉴定的STT细胞。此外，在未麻醉、去大脑和去大脑、脊髓横断的猴子中记录推测的STT细胞。通过从颈脊髓对侧腹外侧索逆向激活这些细胞来进行鉴定。对腓总神经或胫神经施加强度足以在2Hz频率下激活C纤维达15分钟的重复性条件刺激，可极大地抑制由腓肠神经电刺激诱发的C纤维活动以及由有害热诱发的活动。在条件刺激期间抑制作用持续存在，且常常在刺激结束后还会持续20 - 30分钟。尽管去大脑组的平均恢复时间更快，但在去大脑和脊髓横断的动物以及完整麻醉的猴子中均观察到了由周围神经刺激产生的细胞抑制。这表明麻醉剂并未干扰抑制机制。此外，脊髓横断动物中存在抑制作用意味着该抑制作用一定部分依赖于脊髓神经元回路。静脉注射纳洛酮可使抑制恢复阶段显著但轻微缩短。未发现有任何药物能实质性干扰周围条件刺激期间产生的强大抑制作用。这些实验中所使用的实验动物模型似乎适合用于研究周围神经刺激产生镇痛作用的机制。
