Journal
JOURNAL OF NEUROCHEMISTRY
Volume 109, Issue 2, Pages 595-602Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1471-4159.2009.06002.x
Keywords
adenosine; axonal degeneration; guanosine; purine nucleosides; Wallerian degeneration
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Funding
- NIH Neuroscience Blueprint Core [NS057105]
- Hope Center for Neurological Disorders
- Muscular Dystrophy Association
- Ministry of Health, Labour and Welfare of Japan [SHA4431]
- National Institutes of Health [AG013730, NS040745]
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Axonal degeneration is a key component of many neurodegenerative diseases. Injured axons undergo a program of self-destruction termed Wallerian degeneration that is an active, well-regulated process. The pathways leading to axon fragmentation are uncharacterized, but experiments with wld(s) mutant mice led to the discovery that over-expression of NMN adenylyltransferase 1 or treatment with NAD(+) can inhibit axonal degeneration. In this study, we show that the purine nucleosides adenosine and guanosine, but not inosine, inhibit injury-induced axonal degeneration in cultured dorsal root ganglia neurons. Axons can be preserved by adding adenosine within 6 h of the axonal injury. The presence of adenosine was required continuously after the injury to maintain axonal protection. Together these results suggest that adenosine does not alter the neuronal response to injury, but instead inhibits a local axonal pathway necessary for the commitment and/or execution of the axon destructive program.
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