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鸡脑干听觉系统中蛋白质合成的跨神经元调节需要突触激活。

Transneuronal regulation of protein synthesis in the brain-stem auditory system of the chick requires synaptic activation.

作者信息

Hyson R L, Rubel E W

机构信息

Department of Otolaryngology, University of Washington, Seattle 98195.

出版信息

J Neurosci. 1989 Aug;9(8):2835-45. doi: 10.1523/JNEUROSCI.09-08-02835.1989.

Abstract

The cellular mechanisms by which afferents influence their target neurons were investigated using a slice preparation of the chick brain-stem auditory system. Each brain slice contained portions of the auditory nerve and the second-order auditory nucleus, nucleus magnocellularis (NM), bilaterally. NM neurons on one side of the slice were stimulated either orthodromically, via activation of the ipsilateral auditory nerve, or antidromically, via electrical stimulation of their axons. NM neurons on the other side of the slice were not stimulated and served as a within-animal control population. Evoked activity was monitored extracellularly in all preparations. Orthodromic activation of NM neurons for either 1.5 or 3.5 hr resulted in enhanced protein synthesis by these neurons. This result is similar to those of previous in vivo experiments (Steward and Rubel, 1985; Born and Rubel, 1988). When slices were maintained in a medium having low Ca2+ and high Mg2+ concentrations, both synaptic transmission from the auditory nerve to NM and also the difference in protein synthesis between the stimulated and unstimulated sides of the brain were blocked. Antidromic activation of NM neurons did not enhance protein synthesis, but rather resulted in reliably less synthesis by the stimulated cells. Together, these results suggest that activity-dependent release of some "trophic" substance from the auditory nerve is necessary for this form of transneuronal regulation. Electrical activity of the postsynaptic neuron per se is not sufficient for increasing protein synthesis in these cells.

摘要

利用鸡脑干听觉系统的脑片标本,研究了传入神经影响其靶神经元的细胞机制。每片脑片双侧均包含听神经和二级听觉核团——巨细胞神经核(NM)的部分结构。通过激活同侧听神经以顺向刺激脑片一侧的NM神经元,或通过电刺激其轴突以逆向刺激脑片一侧的NM神经元。脑片另一侧的NM神经元不进行刺激,作为动物体内的对照群体。在所有标本中通过细胞外记录来监测诱发活动。对NM神经元进行1.5或3.5小时的顺向激活,会导致这些神经元的蛋白质合成增强。这一结果与之前的体内实验结果相似(Steward和Rubel,1985年;Born和Rubel,1988年)。当脑片置于低钙高镁浓度的培养基中时,从听神经到NM的突触传递以及脑片受刺激侧与未受刺激侧之间的蛋白质合成差异均被阻断。对NM神经元进行逆向激活并未增强蛋白质合成,反而导致受刺激细胞的合成可靠地减少。这些结果共同表明,听神经以活动依赖方式释放某种“营养”物质是这种形式的跨神经元调节所必需的。突触后神经元本身的电活动不足以增加这些细胞中的蛋白质合成。

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