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I 型和 II 型代谢型谷氨酸受体对于雏鸡听觉神经元中核糖体的活性依赖性调节是必需的。

Group I and II metabotropic glutamate receptors are necessary for the activity-dependent regulation of ribosomes in chick auditory neurons.

作者信息

Nicholas Alexander H, Hyson Richard L

机构信息

Department of Psychology, Florida State University, Tallahassee, FL 32306-1270, USA.

出版信息

Brain Res. 2004 Jul 16;1014(1-2):110-9. doi: 10.1016/j.brainres.2004.03.066.

Abstract

Elimination of eighth-nerve activity results in the death of 30% of the neurons in the chick cochlear nucleus, nucleus magnocellularis (NM). One early event in this cell death cascade is the disruption of ribosomes in NM neurons which can be observed within 1 h following deafferentation. These rapid changes in ribosomes can be visualized using Y10B, a monoclonal antibody that recognizes ribosomal RNA. Previous studies using a brain slice preparation of the avian brain stem auditory system have shown that activation of metabotropic glutamate receptors (mGluRs) is necessary for the activity-dependent maintenance of Y10B antigenicity. The purpose of the present study was to determine if group I and/or II mGluRs are necessary for this activity-dependent regulation. This was accomplished by selectively blocking group I or II receptors while unilaterally stimulating the auditory nerve in vitro. In normal media, unilateral stimulation of the auditory nerve resulted in darker Y10B immunolabeling of NM neurons on the stimulated side of the slice. The group I antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA) and the group II antagonists LY341495 and (S)-alpha-ethylglutamic acid (EGLU) all prevented the activity-dependent difference in Y10B immunolabeling. These data suggest that both group I and II mGluRs play vital roles in the activity-dependent regulation of ribosomes in NM.

摘要

消除第八神经活动会导致雏鸡耳蜗核大细胞神经核(NM)中30%的神经元死亡。这种细胞死亡级联反应的一个早期事件是NM神经元中的核糖体破坏,在去传入神经后1小时内即可观察到。使用识别核糖体RNA的单克隆抗体Y10B可以观察到核糖体的这些快速变化。先前使用禽脑干听觉系统脑片制剂的研究表明,代谢型谷氨酸受体(mGluRs)的激活对于Y10B抗原性的活性依赖性维持是必要的。本研究的目的是确定I组和/或II组mGluRs对于这种活性依赖性调节是否必要。这是通过在体外单侧刺激听神经的同时选择性阻断I组或II组受体来实现的。在正常培养基中,单侧刺激听神经会导致切片受刺激侧的NM神经元Y10B免疫标记更深。I组拮抗剂(RS)-1-氨基茚满-1,5-二羧酸(AIDA)以及II组拮抗剂LY341495和(S)-α-乙基谷氨酸(EGLU)均阻止了Y10B免疫标记中活性依赖性差异。这些数据表明,I组和II组mGluRs在NM核糖体的活性依赖性调节中均发挥着重要作用。

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