N-甲基-D-天冬氨酸受体上调：慢性拮抗剂暴露后培养的小鼠皮质神经元的分子研究
NMDA receptor upregulation: molecular studies in cultured mouse cortical neurons after chronic antagonist exposure.
作者信息
Follesa P, Ticku M K
机构信息
Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764, USA.
出版信息
J Neurosci. 1996 Apr 1;16(7):2172-8. doi: 10.1523/JNEUROSCI.16-07-02172.1996.
We examined the possibility of changes in gene expression of the NMDA receptor subunits after chronic antagonist treatment. Exposure of neurons to the NMDA antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP-5) produced an increase in the levels of the R2B mRNA subunit. Concomitant exposure of neurons to AP-5 and NMDA reversed the upregulation. Chronic AP-5 treatment increased the R1 polypeptide, whereas no change was observed in the levels of mRNA encoding the R1 subunit. A more pronounced increase was observed in the R2A/B polypeptides. These data demonstrate that chronic treatment with NMDA antagonists selectively upregulates the NMDA receptor mRNAs and polypeptides. Furthermore, antagonist treatment produced a differential regulation of the R1, R2A, and R2B subunits in cortical neurons.
我们研究了慢性拮抗剂治疗后NMDA受体亚基基因表达变化的可能性。将神经元暴露于NMDA拮抗剂D(-)-2-氨基-5-磷酸戊酸（AP-5）会导致R2B mRNA亚基水平升高。神经元同时暴露于AP-5和NMDA可逆转这种上调。慢性AP-5治疗增加了R1多肽，而编码R1亚基的mRNA水平未观察到变化。在R2A/B多肽中观察到更明显的增加。这些数据表明，NMDA拮抗剂的慢性治疗选择性地上调了NMDA受体的mRNA和多肽。此外，拮抗剂治疗对皮质神经元中的R1、R2A和R2B亚基产生了差异调节。
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