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[四氧嘧啶糖尿病大鼠交感神经节突触传递抑制机制]

[Mechanisms of inhibition of synaptic transmission in the sympathetic ganglia of rats with alloxan diabetes].

作者信息

Pushkarev Iu P

出版信息

Biull Eksp Biol Med. 1978 Sep;86(9):272-4.

PMID:212135
Abstract

In experiments on the isolated superior cervical sympathetic ganglia of rats with alloxan diabetes rhythmic stimulation of preganglionic nerves was effected; summation presynaptic spikes and EPSPs of ganglionic neurons were registered. In rats with moderately severe alloxan diabetes progressive depression of rhythmic ganglion potentials was connected with suppression of the mediator emission to the impulse due to rapid exhaustion of its operational fraction. Rats with severe diabetes displayed also postsynaptic suppression of the ganglionic neurons. Dynamic characteristics of the transmitter turnover assessed on the basis of consideration of the successive patterns of posttetanic potentiation showed insignificant changes in the mediator output and a significant (by 38%) suppression of the mediator reserve per sec in comparison with control.

摘要

在对用四氧嘧啶诱发糖尿病的大鼠离体颈上神经节进行的实验中,对节前神经进行了节律性刺激;记录了神经节神经元的突触前峰电位总和及兴奋性突触后电位。在中度严重四氧嘧啶糖尿病大鼠中,神经节电位的节律性逐渐降低与由于其活性部分快速耗尽导致递质释放对冲动的抑制有关。重度糖尿病大鼠还表现出神经节神经元的突触后抑制。根据强直后增强的连续模式评估的递质周转动态特征显示,与对照组相比,递质输出变化不显著,而每秒递质储备显著(38%)抑制。

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[Mechanisms of inhibition of synaptic transmission in the sympathetic ganglia of rats with alloxan diabetes].[四氧嘧啶糖尿病大鼠交感神经节突触传递抑制机制]
Biull Eksp Biol Med. 1978 Sep;86(9):272-4.
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