Zhang S, Tang J S, Yuan B, Jia H
Department of Physiology, Xi'an Medical University, People's Republic of China.
Neuroscience. 1999;92(3):867-75. doi: 10.1016/s0306-4522(99)00062-7.
In previous studies we have shown that electrical stimulation of the nucleus submedius inhibits the rat radiant heat-induced tail flick reflex, and that this antinociceptive effect is mediated by the ventrolateral orbital cortex and periaqueductal gray. The aim of the present study was to examine whether electrical stimulation of the nucleus submedius could inhibit the rat jaw-opening reflex, and to determine whether electrolytic lesions of the ventrolateral orbital cortex or the periaqueductal gray could attenuate the nucleus submedius-evoked inhibition. Experiments were performed on pentobarbital-anesthetized rats. The jaw-opening reflex elicited by electrical stimulation of the tooth pulp or the facial skin was monitored by recording the evoked digastric electromyogram. Conditioning stimulation was delivered unilaterally to the nucleus submedius 90 ms prior to each test stimulus to the tooth pulp. After that, electrolytic lesions were made in ventrolateral orbital cortex or periaqueductal gray, and the effect of nucleus submedius stimulation on the jaw-opening reflex was re-examined. Unilateral electrical stimulation of nucleus submedius was found to significantly depress the jaw-opening reflex (mean threshold of 28.0+/-1.4 microA, n = 48), and the magnitude of inhibition increased linearly when the stimulus intensity was increased from 20 to 70 microA, resulting in depression of the digastric electromyogram amplitude from 18.4+/-5.4% to 74.0+/-4.9% of the control (P < 0.01, n = 37). The onset of inhibition occured 60 ms after the beginning of nucleus submedius stimulation and lasted about 100 ms, as determined by varying the conditioning-test time interval. Furthermore, ipsilateral lesions of the ventrolateral orbital cortex or bilateral lesions of the lateral or ventrolateral parts of periaqueductal gray eliminated the nucleus submedius-evoked inhibition of the jaw-opening reflex. These data suggest that the nucleus submedius plays an important role in modulation of orofacial nociception, and provide further support for a hypothesis that the antinociceptive effect of nucleus submedius stimulation is mediated by ventrolateral orbital cortex and activation of a descending inhibitory system in the periaqueductal gray.
在先前的研究中,我们已经表明,电刺激中隔核可抑制大鼠辐射热诱导的甩尾反射,并且这种抗伤害感受作用是由腹外侧眶皮质和导水管周围灰质介导的。本研究的目的是检验电刺激中隔核是否能抑制大鼠的张口反射,并确定腹外侧眶皮质或导水管周围灰质的电解损伤是否会减弱中隔核诱发的抑制作用。实验在戊巴比妥麻醉的大鼠身上进行。通过记录诱发的二腹肌肌电图来监测电刺激牙髓或面部皮肤所引发的张口反射。在每次对牙髓进行测试刺激前90毫秒,单侧对中隔核进行条件刺激。之后,在腹外侧眶皮质或导水管周围灰质制作电解损伤,然后重新检测中隔核刺激对张口反射的影响。发现单侧电刺激中隔核可显著抑制张口反射(平均阈值为28.0±1.4微安,n = 48),当刺激强度从20微安增加到70微安时,抑制幅度呈线性增加,导致二腹肌肌电图幅度从对照值的18.4±5.4%降至74.0±4.9%(P < 0.01,n = 37)。通过改变条件刺激 - 测试时间间隔确定,抑制作用在中隔核刺激开始后60毫秒出现,并持续约100毫秒。此外,腹外侧眶皮质的同侧损伤或导水管周围灰质外侧或腹外侧部分的双侧损伤消除了中隔核诱发的对张口反射的抑制作用。这些数据表明,中隔核在口面部伤害感受的调制中起重要作用,并为以下假说提供了进一步支持:中隔核刺激的抗伤害感受作用是由腹外侧眶皮质介导,并通过激活导水管周围灰质中的下行抑制系统实现。