Hyson R L
Department of Psychology, Florida State University, Tallahassee 32306-1051, USA.
Brain Res. 1997 Feb 21;749(1):61-70. doi: 10.1016/s0006-8993(96)01160-2.
Elimination of auditory nerve activity results in death and atrophy of neurons in the cochlear nucleus, nucleus magnocellularis (NM), of the chick. One early event believed to lead to cell death and atrophy is the disruption of ribosomes in the NM neuron. A useful assay for visualizing these ribosomal changes is immunolabeling with the antibody Y10B, which recognizes ribosomal RNA. Activity-dependent changes in Y10B labeling have been observed both in vivo, after unilateral cochlea removal and in vitro after unilateral auditory nerve stimulation. Although it is clear that activity is crucial for maintaining ribosomal integrity, the identity of the important transynaptic signal(s) is not known. It is possible that this trophic signal is glutamate, the neurotransmitter release from the auditory nerve. The present study investigates the role of ionotropic glutamate receptors in the activity-dependent regulation of ribosomes, as measured by the Y10B immunoreactivity. Brain slices containing the auditory nerve and NM on both sides were obtained from hatchling chicks. The auditory nerve on one side of the slice was stimulated for 1 h. The slice was then processed for Y10B immunoreactivity. As expected, greater Y10B immunolabeling was observed on the stimulated side of the slice. Unexpectedly, however, this immunolabeling difference was still observed after blocking NMDA receptors (50 microM DL-APV), non-NMDA receptors (20 microM CNQX), or blocking both ionotropic receptor subtypes (APV and CNQX). This was true even though CNQX eliminated driven postsynaptic potentials. These data suggest that ionotropic glutamate receptors are not necessary for the activity-dependent regulation of ribosomes in NM neurons.
消除听觉神经活动会导致雏鸡的耳蜗核、巨细胞神经核（NM）中的神经元死亡和萎缩。一种被认为会导致细胞死亡和萎缩的早期事件是NM神经元中核糖体的破坏。一种用于观察这些核糖体变化的有效检测方法是用识别核糖体RNA的抗体Y10B进行免疫标记。在单侧耳蜗切除后的体内以及单侧听觉神经刺激后的体外，均观察到Y10B标记的活性依赖性变化。尽管很明显活性对于维持核糖体完整性至关重要，但重要的跨突触信号的身份尚不清楚。这种营养信号可能是谷氨酸，即从听觉神经释放的神经递质。本研究通过Y10B免疫反应性来研究离子型谷氨酸受体在核糖体活性依赖性调节中的作用。从刚孵化的雏鸡获取包含双侧听觉神经和NM的脑片。对脑片一侧的听觉神经进行1小时的刺激。然后对脑片进行Y10B免疫反应性处理。正如预期的那样，在脑片受刺激的一侧观察到更强的Y10B免疫标记。然而，出乎意料的是，在阻断NMDA受体（50微摩尔DL-APV）、非NMDA受体（20微摩尔CNQX）或同时阻断两种离子型受体亚型（APV和CNQX）后，仍观察到这种免疫标记差异。即使CNQX消除了驱动的突触后电位，情况也是如此。这些数据表明，离子型谷氨酸受体对于NM神经元中核糖体的活性依赖性调节并非必需。
