Neural Regeneration Research ›› 2022, Vol. 17 ›› Issue (1): 91-92.doi: 10.4103/1673-5374.314298

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Nogo-A receptor internalization by cyclic adenosine monophosphate in overcoming axonal growth inhibitors after stroke

Rayudu Gopalakrishna*, Charlotte Lin, Mark S. Kindy, William J. Mack   

  1. Department of Integrative Anatomical Sciences, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA (Gopalakrishna R, Lin C) 
    Department of Neurological Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA (Mack WJ)  
    Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA (Kindy MS)
  • Online:2022-01-05 Published:2021-09-18
  • Contact: Rayudu Gopalakrishna, PhD, rgopalak@usc.edu.
  • Supported by:
    This work was supported by NINDS, NIH NS116720 (to RG and WJM).

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Abstract: Currently, there are no clinically proven drugs for recovery from stroke and other neuronal injuries such as traumatic brain injury and spinal cord injury. Recovery therapy requires axonal regeneration, which is inhibited by diverse axonal growth inhibitors, such as Nogo-A, myelin-associated glycoprotein (MAG), oligodendrocyte myelin glycoprotein (OMgp), and chondroitin sulfate proteoglycans (CSPGs) (Chaudhry and Filbin, 2007; Carmichael, 2010; Schwab and Strittmatter, 2014). A cell-surface receptor for Nogo-A, NgR1, mediates the inhibitory action of not only Nogo-A but also other axonal inhibitors (MAG, OMgp, and CSPGs) as well. Intracellular cyclic adenosine monophosphate (cAMP) overcomes neuronal growth inhibition caused by myelin and improves functional recovery from neuronal injuries (Chaudhry and Filbin, 2007). It may block the actions of axonal growth inhibitors by inducing a transcriptional activation of specific genes.  In some cases, cAMP rapidly prevents axonal growth inhibitors from acting through an unknown mechanism (Murray and Shewan, 2008).