Hyson R L
Psychology Department, Florida State University, Tallahassee 32306-1270, USA.
Brain Res. 1998 Nov 2;809(2):214-20. doi: 10.1016/s0006-8993(98)00873-7.
Elimination of auditory nerve activity results in atrophy and death of nucleus magnocellularis (NM) neurons in the chick. One early event in the degeneration of NM neurons is a disruption of their ribosomes. This experiment examines the role of metabotropic glutamate receptors in afferent regulation of ribosomes. The auditory nerve on one side of a chick brainstem slice was stimulated in vitro. Rapid stimulation-dependent changes in ribosomes were visualized by immunolabeling using an antibody, called Y10B, that recognizes ribosomal RNA. In normal media, NM neurons on the stimulated side of the slice show greater Y10B labeling than the unstimulated NM neurons on the opposite side of the same slice. The role of metabotropic glutamate receptors was evaluated by unilaterally stimulating the auditory nerve in media containing the metabotropic glutamate receptor antagonist (RS)-alpha-methyl-4-carboxyphenyl-glycine (MCPG). Addition of MCPG to the bath did not block EPSPs produced by stimulating the auditory nerve. However, MCPG did prevent the stimulation-dependent regulation of ribosomes in NM neurons (as indexed by Y10B labeling). These data suggest that glutamate may play a trophic role in the young auditory system through activation of metabotropic glutamate receptors.
消除听觉神经活动会导致雏鸡的大细胞神经核（NM）神经元萎缩和死亡。NM神经元退化的一个早期事件是其核糖体的破坏。本实验研究了代谢型谷氨酸受体在核糖体传入调节中的作用。在体外刺激雏鸡脑干切片一侧的听觉神经。使用一种名为Y10B的抗体进行免疫标记，该抗体可识别核糖体RNA，从而可视化核糖体快速的刺激依赖性变化。在正常培养基中，切片受刺激一侧的NM神经元比同一切片另一侧未受刺激的NM神经元显示出更强的Y10B标记。通过在含有代谢型谷氨酸受体拮抗剂（RS）-α-甲基-4-羧基苯基甘氨酸（MCPG）的培养基中单侧刺激听觉神经来评估代谢型谷氨酸受体的作用。向浴槽中添加MCPG并不阻断刺激听觉神经产生的兴奋性突触后电位（EPSP）。然而，MCPG确实阻止了NM神经元中核糖体的刺激依赖性调节（以Y10B标记为指标）。这些数据表明，谷氨酸可能通过激活代谢型谷氨酸受体在年轻的听觉系统中发挥营养作用。
