Astrocytes express N-methyl-D-aspartate receptor subunits in development, ischemia and post-ischemia.

Abstract

The expression of the N-methyl-D-aspartate receptor (NMDA-R) in astrocytes is controversial. The receptor is commonly considered neuron-specific. We showed that astrocytes in primary cultures differentially expressed mRNA of NMDA-R subunits, NR1, NR2A and NR2B, in development, ischemia and post-ischemia. One-week-old cultures expressed detectable NR1 mRNA, which fell significantly at 2 weeks and became barely detectable at 4 weeks. NR2A and NR2B mRNA were both significantly up-regulated from 1 to 2 weeks. In 4 weeks, 2 h of ischemia caused a significant up-regulation of NR1 and NR2B mRNA; while 6 h caused down-regulation of NR2A mRNA. Under 3 h of post-ischemia, only NR1 mRNA was increased. Ischemia induced the expression of major NMDA-R effecter, nitric oxide synthase 1, which was unaffected by AMPA-R antagonist CNQX, but dose-dependently inhibited by NMDA-R specific antagonist MK-801. These findings reflected that astrocyte could express inducible functional NMDA receptors without the presence of neurons.

• Authors: Ye Zhou, Hui Li Li, Rui Zhao, Li Tao Yang, Yan Dong, Xin Yue, Yao Ying Ma, Zhuo Wang, Jianguo Chen, Cai Lian Cui, Albert Cheung-Hoi Yu
• Journal: Neurochemical research (Neurochem Res) Vol. 35 Issue 12 Pg. 2124-34 (Dec 2010) ISSN: 1573-6903 [Electronic] United States
• PMID: 21116713 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• RNA, Messenger
• Receptors, N-Methyl-D-Aspartate
• Glutamic Acid
• Hydrogen Peroxide
• Nitric Oxide Synthase Type I
• Nos1 protein, mouse

Topics

• Animals
• Astrocytes (metabolism)
• Brain Ischemia (metabolism, pathology)
• Down-Regulation
• Fluorescent Antibody Technique
• Glutamic Acid (pharmacology)
• Hydrogen Peroxide (pharmacology)
• Mice
• Mice, Inbred ICR
• Nitric Oxide Synthase Type I (metabolism)
• RNA, Messenger (genetics)
• Receptors, N-Methyl-D-Aspartate (genetics, metabolism)
• Up-Regulation