Cell activation and nerve regeneration following peripheral nerve injury

The effect of short time vibration exposure and tourniquet compression on nerve regeneration in rats was studied with special reference to cell activation. One of the hindlimbs was conditioned by either vibration exposure (5 hours / day - 5 consecutive days) or compression (150-300 mmHg for 30-120 minutes), which was followed by a recovery period of 0-7 days. Test crush lesions or a transplantation of a conditioned nerve segment into a freshly made gap in the contralateral nerve (and vice versa after vibration), were performed. Axonal regeneration distances were measured after an additional 3-8 days. Furthermore the reaction of neuronal cellbodies, in the dorsal root ganglia, and non-neuronal cells was studied following compression.

Vibration exposure, and tourniquet compression in particular, increased axonal regeneration lengths after both test crush lesions and transplantation (up to 36%). This so called conditioning effect, which may be regarded as a sign of injury, was in one experiment prevented by treatment with D600, a calcium channel blocker. The non-neuronal cells, which were mainly Schwann cells, increased their proliferation following compression along with an upregulation of the low affinity nerve growth factor receptor (p75). The neuronal cellbodies responded to compression by increased expression of the C-terminal flanking peptide of Neuropeptide Y (CPON).

Thus, tourniquet compression and vibration exposure, which are non-invasive methods, can increase the regenerative capacity of neurons. This requires activation of both Schwann cells and neuronal cellbodies. Conversely, the observed effect of such treatments may be regarded as a potentially harmful alarm reaction in the peripheral nervous system. Whether D600 prevents nerve injury caused by vibration exposure or compression remains to be investigated.