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Glutamate receptors: RNA editing and death of motor neurons
A defect in the editing of the messenger RNA encoding the GluR2 subunit of glutamate AMPA receptors in the spinal motor neurons of individuals affected by ALS will interfere with the correct functioning of the glutamate receptors and may be a contributory cause of neuronal death in ALS patients.
Human spinal motoneurons express low relative abundance of GluR2 mRNA: an implication for excitotoxicity in ALS
The first quantitative measurements of the expression profile of AMPA receptor subunits mRNAs in human single neurons are provided by means of quantitative RT–PCR with a laser microdissector, showing that among the AMPA subunits, GluR2 shared the vast majority throughout the neuronal subsets and tissues examined.
Low editing efficiency of GluR2 mRNA is associated with a low relative abundance of ADAR2 mRNA in white matter of normal human brain
- Y. Kawahara, Kyoko Ito, Hui Sun, I. Kanazawa, S. Kwak
- BiologyThe European journal of neuroscience
- 1 July 2003
The results suggest that Q/R site of GluRs editing is regulated in a regional, and hence presumably cell‐specific, manner and that the GluR2 Q/ R site editing is critically regulated by ADAR2 in human brain.
Slow and selective death of spinal motor neurons in vivo by intrathecal infusion of kainic acid: implications for AMPA receptor‐mediated excitotoxicity in ALS
A rat model of ALS is developed by the long‐term activation of AMPA receptors through continuous infusion of kainic acid (KA), an AMPA receptor agonist, into the spinal subarachnoid space and expression of GluR3 mRNA was selectively up‐regulated in motor neurons but not in dorsal horn neurons of the KA‐infused rats.