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牙髓刺激诱发的下颌张开反射过程中中缝大核神经元的细胞内反应。

Intracellular responses of raphe magnus neurons during the jaw-opening reflex evoked by tooth pulp stimulation.

作者信息

Mason P, Strassman A, Maciewicz R

出版信息

Brain Res. 1986 Aug 6;379(2):232-41. doi: 10.1016/0006-8993(86)90776-6.

Abstract

Neurons in the nucleus raphe magnus (RM) may play an important role in the modulation of nociception. To determine how RM neurons are activated during a nociceptive reflex, the intracellular responses of raphe neurons were studied during the jaw-opening reflex (JOR) elicited by tooth pulp shock in lightly anesthetized cats. Tooth pulp stimulation produces reflex EMG activation of the digastric muscle at a latency of 7-11 ms, resulting in jaw opening. Tooth pulp shock that elicits the JOR also produces an EPSP in a subset of raphe neurons. This EPSP consists of an early small depolarization that occurs at a latency of 10-15 ms followed by a larger depolarization at a latency of 20-60 ms. In all cases the latency to EPSP is longer than the latency to digastric EMG onset. Electrical stimulation of the 4 paws elicits oligosynaptic EPSPs in the same cells at a latency of 16-20 ms. Electrical train stimulation of the midbrain periaqueductal gray region (PAG) suppresses the JOR. Single shock stimulation at the same PAG sites that suppress the JOR evokes monosynaptic EPSPs in the large majority of raphe neurons recorded. In all cases, the threshold for EPSP is below the threshold for suppression of the JOR. The EPSP amplitude is a direct function of PAG stimulus intensity and there is temporal summation of EPSPs evoked by paired PAG shocks. At condition-test intervals of 40-90 ms, train stimulation of PAG suppresses the tooth pulp-evoked EPSP in raphe neurons. The threshold for EPSP suppression occurs at a PAG stimulation intensity below that required for suppression of the JOR. The present findings provide evidence that RM neurons may play an important role in the modulation of the tooth pulp-evoked JOR, but only after the initial withdrawal reflex has occurred.

摘要

中缝大核(RM)中的神经元可能在伤害性感受的调制中发挥重要作用。为了确定在伤害性反射过程中RM神经元是如何被激活的,我们研究了在轻度麻醉的猫中,牙髓冲击诱发的张口反射(JOR)期间中缝神经元的细胞内反应。牙髓刺激在7-11毫秒的潜伏期内产生二腹肌反射性肌电图激活,导致张口。引发JOR的牙髓冲击也会在一部分中缝神经元中产生兴奋性突触后电位(EPSP)。这个EPSP由一个在10-15毫秒潜伏期出现的早期小去极化和随后在20-60毫秒潜伏期出现的较大去极化组成。在所有情况下,EPSP的潜伏期都比二腹肌肌电图开始的潜伏期长。对4只爪子进行电刺激会在相同细胞中以16-20毫秒的潜伏期诱发多突触EPSP。对中脑导水管周围灰质区域(PAG)进行电串刺激会抑制JOR。在抑制JOR的相同PAG部位进行单次电击刺激,在记录的大多数中缝神经元中会诱发单突触EPSP。在所有情况下,EPSP的阈值低于抑制JOR的阈值。EPSP幅度是PAG刺激强度的直接函数,并且由成对的PAG电击诱发的EPSP存在时间总和。在40-90毫秒的条件-测试间隔下,PAG的串刺激会抑制中缝神经元中牙髓诱发的EPSP。EPSP抑制的阈值出现在低于抑制JOR所需的PAG刺激强度下。目前的研究结果提供了证据,表明RM神经元可能在牙髓诱发的JOR的调制中发挥重要作用,但仅在最初的退缩反射发生之后。

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