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Evolution provides different myelin sheathing cells (Oligodendrocyte and Schwann cells) in mammalian CNS and PNS. Damaged neurons in the CNS have little chance of recovery whereas damaged neurons in the PNS have an excellent chance of recovery. When ruptured, olidodendrocytes release Nogo that signals the damaged neuron cell body to stop any attempt at regrowing its axonal stump. Ruptured Schwann cells in the PNS do not release Nogo. Why should nature behave like this? Is it because the wiring density of the CNS is orders of magnitude greater than that of the PNS?

Or could it be because in the PNS the nerve is encased in a perineurial sheath that can readily self-repair and provide a framework for axon regeneration? There doesn't appear to be any similar sheath in the tightly packed CNS. Therefore to prevent unstructured axon regrowth, that could cause chaos in the brain, such a possibility is actively prevented?

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  • $\begingroup$ Your question is a bit unclear. I can't understand your point about how having oligodendrocyte in CNS is detrimental. $\endgroup$
    – WYSIWYG
    Commented Apr 23, 2018 at 9:23
  • $\begingroup$ You are misquoting me, what I said was "to the detriment of CNS neuron damage recovery" which of course is of extreme importance to many CNS injuries not the least being spinal cord injuries. $\endgroup$
    – adlibber
    Commented Apr 23, 2018 at 10:21
  • $\begingroup$ So, you are saying that having two different types of sheathing cells may be a detrimental factor in neuron repair. I still do not get your question. Please edit your question so that it is more clear. Comments should not be used for providing clarifications for many technical and logistic reasons. $\endgroup$
    – WYSIWYG
    Commented Apr 23, 2018 at 10:25
  • $\begingroup$ I think you are taking a huge leap by saying "Oligodendrocytes vs Schwann cells == the reason why CNS damage recovery is more difficult than PNS recovery"... Correlation does not imply causation. $\endgroup$
    – Bryan Krause ♦
    Commented Apr 24, 2018 at 18:12
  • $\begingroup$ Now that’s a very interesting refutation Bryan. How would you interpret the quotations in my answer, the science seems so imperative. $\endgroup$
    – adlibber
    Commented Apr 25, 2018 at 3:19

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I almost got it right. The consensus as of 2018 appears to be that it's a Faustian pact between providing the CNS with our unique mental powers at the cost of poor damage repair. This is not an issue in the PNS where damaged neuron repair is, in the main, impressive.

Quote (1): Principles of Neural Science 5th Ed (2013) (Eric R Kandel et al) “ ... the regenerative capacities in the peripheral nervous system are impressive. In contrast, in the central nervous system regeneration after injury is poor.” “Is it the ability of peripheral axons to regenerate that is unusual, or the inability of central axons to do so? It is in fact the latter.” “Maintaining constancy in the face of small perturbations in connectivity may therefore have the unavoidable consequence of limiting the ability of central connections to regenerate in response to injury. In this view our limited regenerative capacity is the Faustian biological bargain we have made for the possession of many precisely wired circuits that underlie our superior intellectual powers.”

Quote (2): Transl Psychiatry (2017) 7, e1214; doi:10.1038/tp.2017.170 www.nature.com/tp “Reticulon 4 receptor (RTN4R) [aka NgR and NgR1] plays an essential role in regulating axonal regeneration and plasticity in the central nervous system ...”

Quote (3): A.R. Walmsley, D. Bourikas And A.K. Mir, 15 - Myelin Neutralization For Spinal Cord Injury And Stroke, In CNS Regeneration (Second Edition 2008) “ ... the environment of the CNS is highly inhibitory to axonal regeneration and plasticity. In recent years, great advances have been made in our understanding of the molecular components contributing to the inhibitory environment of the CNS. The majority of these have been identified as membrane proteins present in CNS myelin, such as myelin-associated glycoprotein, Nogo-A and oligodendrocyte-myelin glycoprotein, that inhibit neurite outgrowth by binding to the multimeric Nogo-66 receptor (NgR1) complex on the neuron ...”

Quote (4): https://en.wikipedia.org/wiki/Reticulon_4_receptor

Reticulon 4 receptor (RTN4R) also known as Nogo-66 Receptor (NgR) or Nogo receptor 1 is a protein which in humans is encoded by the RTN4R gene. This gene encodes the receptor for reticulon 4, oligodendrocyte myelin glycoprotein and myelin-associated glycoprotein. This receptor mediates axonal growth inhibition and may play a role in regulating axonal regeneration and plasticity in the adult central nervous system.

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