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胍对青蛙脊髓突触传递的影响。

Effects of guanidine on synaptic transmission in the spinal cord of the frog.

作者信息

Grafe P, Sonnhof U

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1977 Dec;301(2):129-34. doi: 10.1007/BF00501427.

Abstract

The effects of guanidine on motoneurons of the isolated frog spinal cord were studied by adding the drug to the solution bathing the cord during intracellular recording. Guanidine (5.10(-4) M) did not alter the membrane potential of motoneurons. The main effect was a marked increase of the amplitudes and frequencies of small spontaneously occurring inhibitory postsynaptic potentials. The hyperpolarizing component of postsynaptic potentials evoked by stimulation of dorsal roots was also enhanced by guanidine. Higher concentrations of guanidine (5.10(-3) M) resulted in a very large and irreversible increase of the small spontaneously occurring inhibitory potentials, which now appeared in a regular, rhythmic pattern. The effects of guanidine could easily be blocked by increasing the magnesium ions (15 mM) in the bath solution. These results indicate that guanidine facilitates the release of an inhibitory transmitter in afferent terminals of the frog spinal cord either by a direct action on these terminals or indirectly by an action on nerve endings impinging on inhibitory interneurons.

摘要

通过在细胞内记录过程中将胍添加到浸泡脊髓的溶液中,研究了胍对离体青蛙脊髓运动神经元的影响。胍(5×10⁻⁴ M)不会改变运动神经元的膜电位。主要作用是显著增加小的自发产生的抑制性突触后电位的幅度和频率。胍还增强了刺激背根诱发的突触后电位的超极化成分。更高浓度的胍(5×10⁻³ M)导致小的自发产生的抑制性电位非常大且不可逆地增加,现在以规则的节律模式出现。通过增加浴液中的镁离子(15 mM),胍的作用很容易被阻断。这些结果表明,胍通过直接作用于青蛙脊髓传入终末或间接作用于影响抑制性中间神经元的神经末梢,促进抑制性递质在这些终末的释放。

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