An iontophoretic analysis of the pharmacologic mechanisms responsible for trigeminal motoneuronal discharge during masticatory-like activity in the guinea pig.
An iontophoretic analysis of the pharmacologic mechanisms responsible for trigeminal motoneuronal discharge during masticatory-like activity in the guinea pig.
复制标题
对豚鼠咀嚼样活动期间三叉神经运动神经元放电的药理机制进行离子电渗分析。
DOI：
10.1152/jn.1990.63.2.356
复制
发表时间：
1990
影响因子：
2.5
通讯作者：
Chandler,SH
中科院分区：
文献类型：
--
作者：
Katakura,N;Chandler,SH
1. 在麻醉豚鼠中研究了兴奋性氨基酸拮抗剂犬尿酸（KYN）和dl -2-氨基-5-磷酸戊酸（APV）以及单胺类5-羟色胺（5-HT）和去甲肾上腺素（NE）在皮质诱导的节律性咀嚼样活动（RMA）中对细胞外记录的开颚运动神经元[二腹肌运动神经元（DIG）]放电的影响。2. 离子电泳应用KYN，广谱氨基酸拮抗剂，抑制了大多数细胞由短脉冲刺激引起的运动神经元放电。相比之下，使用特定的n -甲基- d -天冬氨酸（NMDA）拮抗剂APV的离子电泳通常对短脉冲刺激引起的运动神经元放电没有影响。3. 在重复皮层刺激引起的RMA期间，KYN和APV均抑制了许多细胞的节律性DIG运动神经元放电。4. 这些数据表明，张颌运动神经元上的兴奋性氨基酸受体参与了RMA的激活。我们认为，在短脉冲序列皮层刺激和重复皮层刺激引起的RMA过程中，开颚运动神经元的短潜伏期快速兴奋至少部分是由非nmda受体介导的。这进一步表明，在重复皮质刺激引起的RMA过程中，在开颚运动神经元的膜电位中发生的大振幅、长时间的慢节奏振荡，至少部分是由NMDA受体介导的。5. 低电流（小于20 nA）的NE或5-羟色胺离子化应用在循环触发谷氨酸应用、短脉冲序列皮层刺激和重复皮层刺激引起的RMA时，可促进二腹肌运动神经元放电。这些对运动神经元放电的促进作用在用药后1分钟内开始，在服药后约3分钟达到峰值，持续数分钟，并在10-15分钟内恢复到控制水平。在没有化学或突触激活的情况下，直接使用NE或5-HT不能激活这些运动神经元。然而，在阈下重复皮层刺激过程中，任何一种单胺的离子迁移应用都可以促进并带来阈下节律性运动神经元放电。6. 5-羟色胺拮抗剂甲基塞吉特和α肾上腺受体阻滞剂酚妥拉明的离子渗透应用，分别对5-羟色胺和NE在皮质诱导的RMA中对运动神经元放电的促进作用产生选择性和可逆性阻断。相比之下，离子渗透应用索他洛尔（一种β肾上腺素受体阻滞剂）对ne诱导的RMA的促进作用没有影响。（摘要删节为400字）
1. The effects of iontophoretic application of the excitatory amino acid antagonists kynurenic acid (KYN) and DL-2-amino-5-phosphonovaleric acid (APV), as well as the monoamines serotonin (5-HT) and norepinephrine (NE), on extracellularly recorded jaw opener motoneuron [digastric motoneuron (DIG)] discharge during cortically induced rhythmical masticatory-like activity (RMA) were examined in the anesthetized guinea pig. 2. Iontophoretic application of KYN, a broad-spectrum amino acid antagonist, suppressed the motoneuronal discharge evoked by short pulse train stimulation of the cortex for most cells tested. In contrast, iontophoretic application of APV, a specific N-methyl-D-aspartate (NMDA) antagonist, was usually without effect on the motoneuronal discharge evoked by short pulse train stimulation. 3. During RMA evoked by repetitive cortical stimulation, both KYN and APV suppressed rhythmical DIG motoneuronal discharge in many cells tested. 4. These data suggest that excitatory amino acid receptors on jaw opener motoneurons are involved in activation of RMA. It is proposed that the short-latency rapid excitation of jaw opener motoneurons, which occurs during both short pulse train cortical stimulation and RMA induced by repetitive cortical stimulation, is mediated, at least in part, by non-NMDA receptors. It is further suggested that the large-amplitude, long-duration slow rhythmical oscillations, which occur in the membrane potential of jaw opener motoneurons during RMA induced by repetitive cortical stimulation, are mediated, at least in part, by NMDA receptors. 5. Iontophoretic application of NE or 5-HT with low currents (less than 20 nA) produced a facilitation of digastric motoneuronal discharge during cycle-triggered glutamate application, short pulse train cortical stimulation, and RMA evoked by repetitive cortical stimulation. These facilitatory effects on motoneuronal discharge started within 1 min of drug application, reached a peak at approximately 3 min that persisted for several minutes after the application period, and recovered to control levels within 10-15 min. Direct application of NE or 5-HT, in the absence of chemical or synaptic activation, failed to activate these motoneurons. However, iontophoretic application of either monoamine could facilitate and bring to threshold rhythmical motoneuronal discharges during subthreshold repetitive cortical stimulation. 6. Iontophoretic application of methysergide, a 5-HT antagonist, and phentolamine, an alpha adrenoreceptor blocker, both produced a selective and reversible blockade of the facilitatory effects of 5-HT and NE, respectively, on motoneuronal discharge during cortically induced RMA. In contrast, iontophoretic application of sotalol, a beta adrenoreceptor blocker, had no effect on the NE-induced facilitation of RMA.(ABSTRACT TRUNCATED AT 400 WORDS)