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麻醉对海马引发爆发放大效应的调制作用。

Modulation of hippocampal primed burst potentiation by anesthesia.

作者信息

Engstrom D A, Bennett M C, Stevens K E, Wilson R L, Diamond D M, Fleshner M, Rose G M

机构信息

Medical Research Service, Veterans Administration Medical Center, Denver, CO 80220.

出版信息

Brain Res. 1990 Jun 25;521(1-2):148-52. doi: 10.1016/0006-8993(90)91536-p.

Abstract

This study demonstrates that the anesthetics urethane and pentobarbital differentially affect a low threshold form of long-lasting synaptic plasticity, termed primed burst (PB) potentiation, in the CA1 area of rat hippocampus. PB potentiation was generated by the delivery of a 5-pulse patterned stimulus train, consisting of one priming pulse followed 170 ms later by a burst of 4 pulses at 200 Hz. PB potentiation could not be reliably generated in urethane-anesthetized rats unless stimulus currents were raised to 150% of baseline levels during the stimulus train. In pentobarbital-anesthetized rats, PB potentiation could always be evoked at baseline stimulus intensities. Differences between the anesthetics which could contribute to their varying effects upon PB potentiation are discussed.

摘要

本研究表明,麻醉剂氨基甲酸乙酯和戊巴比妥对大鼠海马CA1区一种低阈值形式的长时程突触可塑性(称为引发爆发(PB)增强)有不同影响。PB增强是通过传递一个由5个脉冲组成的模式化刺激序列产生的,该序列包括一个引发脉冲,随后在170毫秒后紧跟一串频率为200赫兹的4个脉冲。在氨基甲酸乙酯麻醉的大鼠中,除非在刺激序列期间将刺激电流提高到基线水平的150%,否则无法可靠地产生PB增强。在戊巴比妥麻醉的大鼠中,总是可以在基线刺激强度下诱发PB增强。讨论了这两种麻醉剂之间可能导致它们对PB增强产生不同影响的差异。

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