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红核脊髓束及相邻中脑网状结构对家兔延髓呼吸神经元活动及膈神经放电的影响

Influence of rubrospinal tract and the adjacent mesencephalic reticular formation on the activity of medullary respiratory neurons and the phrenic nerve discharge in the rabbit.

作者信息

Schmid K, Böhmer G, Fallert M

机构信息

Department of Physiology, University of Mainz, Federal Republic of Germany.

出版信息

Pflugers Arch. 1988 Nov;413(1):23-31. doi: 10.1007/BF00581224.

Abstract

Suprapontine brain sites acting on the central respiratory system have been demonstrated to give rise to inspiratory as well as expiratory facilitatory effects. In the present study the inspiratory inhibitory effect which has been reported in the cat to be elicited consistently by electrical stimulation of the rubrospinal tract and the adjacent mesencephalic reticular formation was examined in the urethane-anaesthetized rabbit. Stimulation of these sites with single electrical shocks of moderate intensity induced a short latency (onset after 3.0 ms) transient (duration: 29 ms) inhibition of the phrenic nerve activity (PHR). Short volleys of stimuli applied in mid- to late-inspiration led to a premature off-switch of inspiration. The extracellularly recorded discharge activity of the different types of medullary respiration-related units (RRU) reflected these alterations, accordingly. Axonal connections of RRU with mesencephalic structures were evaluated. Examination of orthodromic responses of medullary RRU to stimulation of this pathway revealed that most bulbospinal inspiratory neurons (10 out of 13) were paucisynaptically inhibited after short latency (at least 1.2 ms). The conduction time from bulbospinal inspiratory neurons to the recording site of PHR was 1.6 ms. Thus, a disynaptic pathway--including bulbospinal inspiratory neurons--is suggested inducing inspiratory inhibition 3.0 ms after single shock midbrain stimulation. This inhibition results in disfacilitation of phrenic motoneurons. The fact that extensive electrolytic lesions of the pneumotaxic center in rostral pons did not abolish the observed inspiratory inhibitions excludes these structures from being involved.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

已证明作用于中枢呼吸系统的脑桥以上脑区会产生吸气和呼气促进作用。在本研究中,在氨基甲酸乙酯麻醉的家兔身上,研究了猫中通过电刺激红核脊髓束和相邻的中脑网状结构持续引发的吸气抑制作用。用中等强度的单次电刺激这些部位,可诱导膈神经活动(PHR)出现短暂潜伏期(3.0毫秒后开始)的短暂(持续时间:29毫秒)抑制。在吸气中期至后期施加短串刺激会导致吸气提前终止。相应地,不同类型的延髓呼吸相关单位(RRU)的细胞外记录放电活动反映了这些变化。评估了RRU与中脑结构的轴突连接。检查延髓RRU对该通路刺激的顺行反应发现,大多数延髓脊髓吸气神经元(13个中有10个)在短潜伏期(至少1.2毫秒)后受到少突触抑制。从延髓脊髓吸气神经元到PHR记录部位的传导时间为1.6毫秒。因此,提示存在一条包括延髓脊髓吸气神经元的双突触通路,在中脑单次刺激后3.0毫秒诱导吸气抑制。这种抑制导致膈运动神经元的去易化。脑桥前部呼吸调整中枢广泛的电解损伤并未消除观察到的吸气抑制,这一事实排除了这些结构参与其中。(摘要截短于250字)

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