刺尾鱼毒素对大鼠神经肌接头突触传递的影响

目的和方法：在大鼠不均匀牵张膈肌标本（INSMP）上,用传统的微电极胸内记录方法。研究MTX对大鼠膈肌膈神经突触传递的影响。结果：①浴槽给予TMX（10μg/L）,18.0min后,串刺激神经突然不能产生串终极电位（EFP）。 随后,突触后膜开始逐渐去极化,最大去极化27．0mV。62.7min后小终板电位（mEPP)频率逐渐增高,到70．3min达到最高频率,比给药前增加了32倍。这种高频的MEPP可以持续20－30min;②提前20min溶槽给予20μmol／L的L－型Ca^2 通道阻断剂异搏定（Veranpamil),然后给予MTX（10μg/L,78.5min后串刺激神经不能产生串EPP,与单给MTX相比时间明显延长（P＜0．01）。而突触后膜最大去极化幅度、mEPP频率增高时间及最高频率与单给MTX相比没有明显区别。结论：ＭＴＸ对神经肌头突触传递的阻断作用首先表现在神经纤维不能兴奋,这种作用可以部分被L－型Ca^2 通道阻断剂Verapamil所对抗。随后出现突触后膜去极化、mEPP频率显著增高,Verapamil对此没有明显对抗作用。     

Effects of berberine,glaucine, stephaglabrine,and sanguirythrine on neuromuscular transmission

The effects of certain alkaloid (glaucine, stephaglabrine, and sanguirythrine) on parameters of neuromuscular transmission follow a complex pattern and are thought likely to operate via two or more different mechanisms. These alkaloids, in common with berberine, reduced the amplitude of miniature potentials at the frog neuromuscular junction. All four concentrations reduced and raised miniature potential rate at low and high concentrations respectively — a very marked action in the case of sanguirythrine, producing virtually a 100-fold increase, probably due to its uncoupling effect on oxidative phosphorylation at the mitochondria of the nerve endings. Sanguirythrine and stephaglabrine both gave rise to repeated muscular contraction which matches their anticholinesterase activity. High glaucine concentrations also induced contraction of the muscles.Institute for Hydrobiontic Substance Research, Soviet Ministry of Health, Moscow. Translated from Neirofiziologiya, Vol. 23, No. 2, pp. 131–135, March–April, 1991.     

Effects of calcitonin gene-related peptide on neuromuscular transmission in the isolated rat diaphragm

The present study was undertaken to investigate a possible interaction between the cholinergic nerve neurotransmitter and CGRP on neuromuscular transmission in the isolated rat diaphragm. Electrical stimulation of the isolated phrenic nerve resulted in twitch contractions which were dose-dependently potentiated by CGRP in concentrations ranging from 1.2 x 10(-9) M to 3 x 10(-7) M. The potentiating action of CGRP (3 x 10(-7) M) disappeared in about 25 min. The same dose of CGRP 40 min later produced an augmentation of contraction amplitude similar to that observed prior to the administration of CGRP. The action of CGRP was dependent upon the stimulation pulse width ranging from 0.2 to 1.0 msec. Rat calcitonin (4.5 x 10(-7) M) caused a minimal change in the amplitude of twitch contractions. CGRP had no effect on the quiescent striated muscle. Twitch responses to direct electrical stimulation were also enhanced by CGRP (6 x 10(-8) M-6 x 10(-7) M) in the absence and presence of 10(-5) M d-tubocurarine. These results suggest that CGRP modulates the action of acetylcholine at the motor end plates of striated muscle.     

Stress-induced thermoprotection of neuromuscular transmission

Environmental stresses such as high temperature or low levelsof oxygen can lead to structural destabilization of cells, disruptionof cellular processes, and, in extreme cases, death. Previousexperience of sub-lethal stress can lead to protection duringa subsequent stress that may otherwise have been lethal. Synapsesare particularly vulnerable to extreme environmental conditionsand failure of function at this level may be the primary causeof organismal death. Prior heat shock induces enhanced thermotoleranceat neuromuscular junctions in the locust extensor tibiae muscleand in abdominal muscles of larval Drosophila. Synaptic thermoprotectionis associated with an increase in short-term plasticity at thesesynapses. Prior anoxic coma in locusts induces synaptic thermotolerancesuggesting that the same protective pathways are activated.It is well established that diverse forms of stress induce theupregulation of cellular chaperones (heat shock proteins; HSPs)that mediate acquired protection. The mechanisms underlyingHSP-mediated synaptic protection are currently unknown but evidenceis accumulating that stabilization of the cytoskeleton may playan important role.     

The effects of heptaminol chlorhydrate on neuromuscular transmission

6-Amino-2-methyl-2-heptanol chlorhydrate, heptaminol chlorhydrate, blocks the response to indirect stimulation of the mouse diaphragm in vitro. This effect is due to a dose-dependent pre- and post-synaptic block of neuromuscular transmission starting at 1 mM heptaminol (HEPT). The complete block of neuromuscular transmission occurs at 10 mM. At 2 mM, the decrease in quantal size is more significant in the presence of d-tubocurarine than when the extracellular calcium is lowered. At this concentration, heptaminol also prolongs the depolarization time of the motor end plate potential. Slightly higher concentrations of heptaminol produce a decrease in quantal content. This latter effect is associated with an increase in synaptic delay.     

神经营养因子对神经肌肉接头传递的调制作用

运动单位由运动神经元及其支配的肌纤维组成。神经肌肉接头(neuromuscular junction,NMJ)传递受到严密的调节,因而能和运动单位的活动协调一致。在NMJ,神经调制物质的释放与运动单位的活动有关,并能决定突触传递的效能。脑源性神经营养因子(brain—derived neurotrophic factor,BDNF)和神经营养因子4(neurotrophin-4,NT-4)由运动神经末梢和肌纤维产生。肌肉释放营养因子受肌肉活动调节。在NMJ,BDNF和NT-4通过激活酪氨酸激酶B受体(tyrosine kinase receptor B,TrkB),能加强自发性和诱导性的突触活动。突触前Ca^2 量的迅速增加或突触胞吐过程的易化,都能增加突触囊泡的释放,从而改善NMJ的突触传递。事实上,BDNF能促进突触前细胞内Ca^2 的释放,TrkB的激活也能通过有丝分裂活化蛋白激酶,引起突触素I(synapsinI)的磷酸化,进而增加可释放的突触囊泡的数量。在NMJ,神经营养因子还能通过影响神经调节素(neuregulin)或其他神经源性调制物质的局部释放,对接头传递进行调节。本文对近年来在NMJ突触传递的调节,运动单位的NMJ特性以及神经营养因子对突触传递效能的影响等方面的研究进展做一综述。     

Glutamatergic modulation of vertebrate neuromuscular transmission

The paper is devoted to the analysis of evidence pointing to presence of glutamatergic modulation of vertebrate neuromuscular transmission. The data on the glutamate's origin and release in the endplate region as well as on the presence of specific glutamate receptors are discussed. The effects of glutamate on different types of acetylcholine secretion in the synapses of amphibians and mammals are described. The question of possible physiological role of glutamatergic modulation of neuromuscular transmission is discussed.     

Action of some surfactants on neuromuscular transmission in frogs

The effect of bile salts, saponin, and Tween-80 on miniature end-plate potentials and electrotonic potentials of frog muscle fibers was studied. During the action of bile salts in a concentration of 10^–4 g/ml the frequency of the synaptic potentials rose sharply. Their amplitude also increased. The input resistance of the muscle fiber decreased during the action of these substances. With an increase in their concentration to 10^–3 g/ml bile salts caused an initial increase in frequency of the spontaneous synaptic potentials followed by their depression and complete disappearance. Tween-80 caused no appreciable change in synaptic activity, whereas saponin inhibited it. Lowering the external calcium ion concentration by two to eight times had no influence on the stimulating effect of bile salts, but the total removal of calcium reduced it. The substances tested stimulated secretion of acetylcholine from the nerve endings, probably through changes caused in the structure of the presynaptic membrane.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 8, No. 3, pp. 305–310, May–June, 1976.     

Action of thiamine on neuromuscular transmission in the frog

The action of thiamine on neuromuscular transmission in the frog sartorius muscle was investigated. It was found that thiamine at a concentration of 1×10^–14 to 1×10^–4 M increases transmitter secretion at the nerve endings. This is demonstrated by the increased frequency, amplitude, and quantal content of miniature endplate potentials, and is due to the enhanced likelihood of transmitter release. The role of thiamine in regulating synaptic transmission and the mechanism of its interaction with thiamine-sensitive receptors are examined.A. V. Palladin Institute of Biochemistry, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 17, No. 6, pp. 794–800, November–December, 1985.