Pronounced changes in the activity of nociceptive modulatory neurons in the rostral ventromedial medulla in response to prolonged thermal noxious stimuli.

Pronounced changes in the activity of nociceptive modulatory neurons in the rostral ventromedial medulla in response to prolonged thermal noxious stimuli.
复制标题

延髓头端腹内侧伤害性调节神经元的活性显着变化,以响应长时间的热伤害刺激。

DOI:
10.1152/jn.1994.72.3.1161
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发表时间:
1994
影响因子:
2.5
通讯作者:
Fields,HL
Fields,HL
中科院分区:
医学3区
文献类型:
--
作者:
Morgan,MM;Fields,HL

文献摘要

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1.抑制伤害性感觉的大脑区域可以被各种环境刺激激活,包括长时间的伤害性刺激。本研究观察了长时间伤害性刺激对延髓吻侧腹内侧区伤害性调制神经元活动的影响。这些神经元被称为开细胞和离细胞,因为它们分别在与伤害性感受器反射相关的活动中爆发和暂停,已被证明分别促进和抑制伤害性感受。2.在氟烷或巴比妥酸盐轻度麻醉的大鼠暴露于50℃的高温(50℃水)中,评估了开细胞和离细胞的单位活性。这种持续的伤害性刺激导致无论麻醉剂(氟烷或巴比妥酸盐)或刺激位置(后爪或尾巴)如何,细胞内活动增加,细胞外活动减少。3.令人惊讶的是,尽管RVM细胞活动持续变化,但长时间的伤害性刺激根据用于评估伤害性感觉的反射而引起不同的影响。当尾巴浸入热水中时,后爪回缩反射被促进,而当后爪浸入热水中时,尾巴甩动反射被抑制(见前文)。利多卡因灭活RVM可缩短两种反射的潜伏期,但对伤害性条件反射产生的甩尾抑制无影响。相反,利多卡因失活RVM完全逆转了尾热所产生的后爪反射易化,表明RVM ON细胞参与了这一反射的易化。4.这些数据表明,RVM神经元对伤害性刺激的反应是一致的,无论是短时间的还是长时间的:细胞上的活动增加,细胞外的活动减少。此外,伤害性刺激产生的RVM对细胞的激活足以增强一些伤害性反射,而RVM以外的神经结构似乎介导了长时间伤害性刺激产生的抗伤害效应。
1. Brain regions that inhibit nociception can be activated by various environmental stimuli, including prolonged noxious stimuli. The present study tested the effect of such a prolonged noxious stimulus on the activity of nociceptive modulatory neurons in the rostral ventromedial medulla (RVM). These neurons, called ON- and OFF-cells because of their respective burst and pause in activity associated with nocifensor reflexes, have been shown to facilitate and inhibit nociception, respectively. 2. Single-unit activity of ON- and OFF-cells was assessed in lightly halothane- or barbiturate-anesthetized rats exposed to prolonged noxious heat (50 degrees C water). This prolonged noxious stimulus caused an increase in ON-cell and a decrease in OFF-cell activity regardless of anesthetic (halothane or barbiturate) or stimulus location (hindpaw or tail). 3. Surprisingly, and despite the consistent changes in RVM cell activity, the prolonged noxious stimulus caused different effects depending on the reflex used to assess nociception. The hindpaw withdrawal reflex was facilitated when the tail was immersed in hot water, whereas the tail flick reflex was inhibited when the hindpaw was immersed in hot water (see preceding manuscript). Lidocaine inactivation of the RVM shortened the latency for both reflexes but had no effect on tail flick inhibition produced by the noxious conditioning stimulus. In contrast, lidocaine inactivation of the RVM completely reversed the hindpaw reflex facilitation produced by tail heat, indicating the involvement of RVM ON-cells in facilitation of this reflex. 4. These data demonstrate that RVM neurons respond in a consistent manner to noxious stimuli whether applied for a brief or prolonged time: ON-cell activity increases and OFF-cell activity decreases. Moreover, the activation of RVM ON-cells produced by a noxious stimulus is sufficient to enhance some nocifensor reflexes, whereas neural structures other than the RVM appear to mediate the antinociceptive effects produced by a prolonged noxious stimulus.