Abstract
Schwann cells produce myelin sheath around peripheral nerve axons. Myelination is critical for rapid propagation of action potentials, as illustrated by the large number of acquired and hereditary peripheral neuropathies, such as diabetic neuropathy or Charcot-Marie-Tooth diseases, that are commonly associated with a process of demyelination.
Highlights
In the peripheral nervous system (PNS), Schwann cells (SCs) are responsible for myelin production, which contributes to axonal protection and allows for efficient action potential transmission [1,2]
The beam cross time was significantly increased at 11 ± 2 seconds in the nerve injury+vehicle group mice whereas the cross time of control animals remained at 5 ± 1 seconds
Concerning the nerve injury+RSV group, the beam cross times was increased at 8 ± 1 seconds but this increase was not significant compared to the control group
Summary
In the peripheral nervous system (PNS), Schwann cells (SCs) are responsible for myelin production, which contributes to axonal protection and allows for efficient action potential transmission [1,2]. Acquired and hereditary demyelinating diseases of the PNS are numerous and affect an increasing number of people [3]. The etiologies of acquired and hereditary peripheral nerve diseases are diverse, but they all result in demyelination and subsequent neuronal death. It has been reported that at least 50% of diabetic patients develop one or several forms of diabetic neuropathy within 25 years after diagnosis [7]. This neuropathy affects both myelinated SCs and peripheral axons/neurons, leading to changes in nerve conduction, and it is often associated with demyelination in the long term [9]. The physiological and molecular mechanisms that lead to these nerve defects remain unclear
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