Reduced capabilities of synaptic transmission in aged rats

Reduced capabilities of synaptic transmission in aged rats
复制标题

老年大鼠突触传递能力下降

DOI:
10.1016/0014-4886(79)90210-3
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发表时间:
1979
影响因子:
5.3
通讯作者:
Dean O. Smith
Dean O. Smith
中科院分区:
医学2区
文献类型:
--
作者:
Dean O. Smith

文献摘要

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在老年和年轻的对照组大鼠膈神经-膈肌神经肌肉接头处的突触传递进行了研究;它们的年龄分别为24至26个月和12至13个月。发现老年动物的膈肌细胞静息电位始终低于对照组。膜输入电阻和电容没有显着差异。老年大鼠微型终板电位(MEPPs)的发生率是对照组的1.75倍;然而,在两种情况下,连续MEPPs发生时间之间的间隔分布均呈指数分布。在Mg 2+阻断制剂中,观察到易化和强直后增强;从两个年龄组获得的数据之间的差异不显着。在箭毒阻断制剂中,突触抑制发生在重复神经刺激期间。老年动物的抑郁更严重;这种差异是一致的,与刺激率无关。重复的神经刺激导致动作电位传导阻滞的突触前末梢的两个年龄组,然而,失败发生在较低的频率和较短的时间在老年动物的刺激。阻滞似乎与膜去极化有关。我们的结论是,维持传输的能力是老年大鼠的神经肌肉接头减少,这可能是衰老过程中观察到的突触结构恶化的基础。
Synaptic transmission at the neuromuscular junction of the rat phrenic nerve-diaphragm muscle was studied in aged and young, control rats; their ages were 24 to 26 and 12 to 13 months, respectively. The resting potential of the diaphragm muscle cells was found to be consistently lower in the old animals than in the controls. Membrane input resistance and capacitance were not significantly different. The rate of occurrence of miniature end-plate potentials (MEPPs) in old rats was 1.75 times higher than in the controls; the distribution of intervals between the times of occurrence of successive MEPPs was exponential in both cases, however. In Mg2+-blocked preparations, facilitation and posttetanic potentiation were observed; differences between data obtained from both age groups were not significant. In curare-blocked preparations, synaptic depression occurred during repetitive nerve stimulation. The depression was more severe in the aged animals; this difference was consistent and independent of the rate of stimulation. Repetitive nerve stimulation led to action potential conduction block in the presynaptic terminals of both age groups; however, failure occurred at lower frequencies and shorter times of stimulation in the aged animals. The block appeared to be associated with membrane depolarization. We conclude that the capability to sustain transmission is diminished at the neuromuscular junction of aged rats; this could underlie the deterioration of synaptic structures observed during senescence.