Nagata Tomonari, Suzuki Hidehiro, Zhang Rihui, Ozaki Makoto, Kawakami Yoriko
Department of Anesthesiology, Tokyo Women's Medical University, Tokyo, Japan.
Exp Brain Res. 2003 Apr;149(4):505-11. doi: 10.1007/s00221-003-1381-0. Epub 2003 Mar 4.
We characterized nociceptive discharges induced by mechanical stimulation and the modulating effects of orphanin FQ on noxious responses in the rat brain stem gigantocellular reticular nucleus (Gi). A pressure pulse of constant force and rising rate was delivered by a mechanical stimulator with feedback control, allowing responses to be analyzed statistically. A pressure pulse of 300 g, which evoked C-fiber mediated nerve responses, was delivered to the tail. Two excitatory (45/58) and one inhibitory (13/58) types of extracellular unit discharges were recorded in Gi. One of the excitatory types was a phasic discharge (13/45) elicited at the onset and/or the end of stimulation. Latencies of the phasic discharges (0.104+/-0.1 s) were shorter than those of other type (tonic) discharges (0.43+/-0.2 s). The tonic discharges (32/45), which frequently persisted past the end of stimulation without adaptation, were classified into two groups. The first group of tonic type units (23/45) was high threshold, like nociceptive specific neurons in the primary sensory cortex, while the second group of neurons (9/45) responded to a wide range of stimulus intensities. The mean frequency, response duration and spike numbers gradually increased with stimulus intensity change in all nine neurons. The neurons encode mechanical stimulus intensity with discharge frequency, response duration and evoked spike numbers. Local injection of orphanin FQ (200 ng/2 microl) changed high threshold tonic type spike numbers in a biphasic manner, i.e., there was an early phase suppression (5-30 min, p=0.016) and a late phase enhancement (30-60 min, p=0.027). In contrast, phasic type discharges did not show an altered discharge pattern in response to orphanin FQ. Thus, orphanin FQ affects small fiber-mediated nociceptive responses and may behave as a complex modulator of pain systems in the brain stem.
我们对机械刺激诱发的伤害性放电以及孤啡肽FQ对大鼠脑干巨细胞网状核(Gi)中伤害性反应的调节作用进行了表征。通过具有反馈控制的机械刺激器施加恒定力和上升速率的压力脉冲,从而能够对反应进行统计学分析。将诱发C纤维介导的神经反应的300 g压力脉冲施加于尾部。在Gi中记录到两种兴奋性(45/58)和一种抑制性(13/58)类型的细胞外单位放电。其中一种兴奋性类型是在刺激开始和/或结束时诱发的相位性放电(13/45)。相位性放电的潜伏期(0.104±0.1秒)短于其他类型(紧张性)放电的潜伏期(0.43±0.2秒)。紧张性放电(32/45)在刺激结束后经常持续存在且无适应性变化,被分为两组。第一组紧张性类型单位(23/45)具有高阈值,类似于初级感觉皮层中的伤害性特异性神经元,而第二组神经元(9/45)对广泛的刺激强度有反应。在所有九个神经元中,平均频率、反应持续时间和峰电位数量随刺激强度变化而逐渐增加。这些神经元通过放电频率、反应持续时间和诱发的峰电位数量对机械刺激强度进行编码。局部注射孤啡肽FQ(200 ng/2微升)以双相方式改变高阈值紧张性类型的峰电位数量,即存在早期抑制(5 - 30分钟,p = 0.016)和晚期增强(30 - 60分钟,p = 0.027)。相比之下,相位性放电对孤啡肽FQ未表现出放电模式的改变。因此,孤啡肽FQ影响小纤维介导的伤害性反应,并且可能作为脑干中疼痛系统的复杂调节剂发挥作用。