Intracellular analysis of trigeminal motoneuron rhythmical activity during stimulation of pontomedullary reticular formation in anesthetized guinea pig.

Intracellular analysis of trigeminal motoneuron rhythmical activity during stimulation of pontomedullary reticular formation in anesthetized guinea pig.
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麻醉豚鼠脑桥延髓网状结构刺激过程中三叉神经运动神经元节律活动的细胞内分析。

DOI:
10.1152/jn.1989.62.6.1225
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发表时间:
1989
影响因子:
2.5
通讯作者:
Goldberg,LJ
Goldberg,LJ
中科院分区:
医学3区
文献类型:
--
作者:
Gurahian,SM;Chandler,SH;Goldberg,LJ

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1.本实验观察了重复电刺激网状结构的脑桥尾侧核和延髓细胞核(PnC-Gi)对开颌运动神经元和闭颌运动神经元的影响。在小于90微安的电流强度下以75 Hz刺激PnC-Gi。2.通过40 Hz重复咀嚼皮层刺激,在开颌运动神经元中有节奏地发生长持续时间去极化膜电位[兴奋性咀嚼驱动电位(E-MDP)]和在闭颌运动神经元中长持续时间超极化膜电位[抑制性咀嚼驱动电位(I-MDP)]。这些电位被PnC-Gi刺激完全抑制。PnC-Gi刺激还抑制了由相同的重复皮层刺激诱发的开颌运动神经元中的短持续时间、刺激锁定的去极化[兴奋性突触后电位(EPSP)]和开颌运动神经元中的短持续时间、刺激锁定的超极化[抑制性突触后电位(IPSP)]。3.短脉冲串(3个脉冲; 500 Hz)刺激咀嚼区的皮质在没有节奏的下颌运动激活短潜伏期少突触皮质三叉神经通路,并诱发短持续时间的EPSP和IPSP在下颌张开和关闭运动神经元,分别。同样的PnC-Gi刺激,完全抑制节奏的MDP,和刺激锁定的PSP诱发的咀嚼区的皮层的重复刺激,产生的PSP振幅平均减少22%和17%的下颌关闭和打开运动神经元,分别。4. PnC-Gi刺激对逆向二胃场电位的振幅或细胞内记录的逆向二胃动作电位产生最小的影响。此外,PnC-Gi刺激对无节律性下颌运动(RJMs)的下颌张开或下颌闭合运动神经元膜静息电位几乎没有影响。PnC-Gi刺激引起的下颌张开器和更近的运动神经元在RJMs的情况下的电导脉冲产生可变的影响。5.这些结果表明,在PnC-Gi刺激过程中,开放和关闭运动神经元中皮质诱发的MDP的强大抑制很可能不是三叉神经运动神经元突触后抑制的结果。有人提出,这种抑制是由于抑制活动的神经元负责咀嚼节奏的产生。
1. The effects of repetitive stimulation of the nucleus pontis caudalis and nucleus gigantocellularis (PnC-Gi) of the reticular formation on jaw opener and closer motoneurons were examined. The PnC-Gi was stimulated at 75 Hz at current intensities less than 90 microA. 2. Rhythmically occurring, long-duration, depolarizing membrane potentials in jaw opener motoneurons [excitatory masticatory drive potential (E-MDP)] and long-duration hyperpolarizing membrane potentials [inhibitory masticatory drive potentials (I-MDP)] in jaw closer motoneurons were evoked by 40-Hz repetitive masticatory cortex stimulation. These potentials were completely suppressed by PnC-Gi stimulation. PnC-Gi stimulation also suppressed the short-duration, stimulus-locked depolarizations [excitatory postsynaptic potentials (EPSPs)] in jaw opener motoneurons and short-duration, stimulus-locked hyperpolarizations [inhibitory postsynaptic potentials (IPSPs)] in jaw closer motoneurons, evoked by the same repetitive cortical stimulation. 3. Short pulse train (3 pulses; 500 Hz) stimulation of the masticatory area of the cortex in the absence of rhythmical jaw movements activated the short-latency paucisynaptic corticotrigeminal pathways and evoked short-duration EPSPs and IPSPs in jaw opener and closer motoneurons, respectively. The same PnC-Gi stimulation that completely suppressed rhythmical MDPs, and stimulus-locked PSPs evoked by repetitive stimulation to the masticatory area of the cortex, produced an average reduction in PSP amplitude of 22 and 17% in jaw closer and opener motoneurons, respectively. 4. PnC-Gi stimulation produced minimal effects on the amplitude of the antidromic digastric field potential or on the intracellularly recorded antidromic digastric action potential. Moreover, PnC-Gi stimulation had little effect on jaw opener or jaw closer motoneuron membrane resting potentials in the absence of rhythmical jaw movements (RJMs). PnC-Gi stimulation produced variable effects on conductance pulses elicited in jaw opener and closer motoneurons in the absence of RJMs. 5. These results indicate that the powerful suppression of cortically evoked MDPs in opener and closer motoneurons during PnC-Gi stimulation is most likely not a result of postsynaptic inhibition of trigeminal motoneurons. It is proposed that this suppression is a result of suppression of activity in neurons responsible for masticatory rhythm generation.