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用胍或四乙铵处理的青蛙神经肌肉接头处递质释放的统计参数。

Statistical parameters of transmitter release at frog neuromuscular junctions treated with guanidine or tetraethylammonium.

作者信息

Volle R L, Branisteanu D D

出版信息

J Pharmacol Exp Ther. 1976 Jun;197(3):653-61.

PMID:6788
Abstract

Transmitter release at Mg++ -depressed frog neuromuscular junctions can be described using binomial statistics. The number of quanta (m) released by the nerve terminal action potential is directly proportional to the mean probability (p) that a quantum will be released and the number of quanta available for release (n). Guanidine or tetraethylammonium (TEA) increased m and n, but had no effect on p. At junctions depressed by d-tubocurarine, both compounds enhanced the amplitude of the initial end-plate potential, caused an accelerated rate of fade of end-plate potential amplitudes and raised the steady-state level of end-plate potential amplitude. This finding was interpreted to mean that guanidine and TEA increased transmitter mobilization and may be related to the increase by the compounds of the parameters n. If so, then the data support the idea that n represents the number of quanta available for release rather than the number of transmitter release sites in the terminal membrane. Neither compound affected the power relationship between [Ca++]o and transmitter release. When plotted on a double logarithmic basis, the slope of the line relating [Ca++]o to increased transmitter release was 3.7, a relationship not altered by the drugs. Thus, the compounds had no effect on the fundamental interaction between Ca++ and transmitter release sites. In contrast to [Ca++]o, the power relationship between increased transmitter release and the concentration of drug in the bathing solution was 0.69 for guanidine and 0.84 for TEA. Because of this finding, it was concluded that the compounds increased transmitter release by mechanisms other than or in addition to increasing Ca++ conductance.

摘要

在镁离子抑制的青蛙神经肌肉接头处,递质释放可用二项式统计来描述。神经末梢动作电位释放的量子数(m)与量子释放的平均概率(p)以及可供释放的量子数(n)成正比。胍或四乙铵(TEA)增加了m和n,但对p没有影响。在被d - 筒箭毒碱抑制的接头处,这两种化合物都增强了终板电位初始幅度,导致终板电位幅度衰减速率加快,并提高了终板电位幅度的稳态水平。这一发现被解释为胍和TEA增加了递质动员,可能与化合物使参数n增加有关。如果是这样,那么数据支持这样的观点,即n代表可供释放的量子数,而不是终末膜中递质释放位点的数量。这两种化合物都不影响细胞外钙离子浓度([Ca++]o)与递质释放之间的幂关系。当以双对数坐标绘制时,将[Ca++]o与递质释放增加相关的直线斜率为3.7,这种关系不受药物影响。因此,这些化合物对钙离子与递质释放位点之间的基本相互作用没有影响。与[Ca++]o相反,递质释放增加与浴液中药物浓度之间的幂关系,胍为0.69,TEA为0.84。基于这一发现,得出的结论是,这些化合物通过增加钙离子电导以外的机制或除增加钙离子电导之外还通过其他机制增加递质释放。

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