Recovery from peripheral nerve damage is a slow and often incomplete process that may leave behind lasting deficits including severe disability. The poor functional recovery is due in part to limited regrowth of axons. For example, after nerve transection, only 10% of axons from the proximal stump may eventually reach their targets. Axon regrowth can be regulated by various growth factors and by intrinsic 'braking' mechanisms. A recent report in Nature Communications (5, 3670; 2014) shows how manipulating one of these molecular brakes can enhance nerve growth and improve functional motor and sensory recovery after injury.
The study was carried out by Douglas Zochodne and colleagues (University of Calgary, Canada), who used small interfering RNA to reduce expression of the retinoblastoma protein (Rb) in rats and mice with damage to their sciatic nerves. Rb inactivation allowed more axons to grow farther across the damaged area after nerve transection and enabled more rapid recovery of hindpaw grip strength, earlier resolution of mechanical hypoalgesia and prevention of thermal hyperalgesia after nerve crush. Zochodne explained in a press release that Rb acts “as a brake—preventing nerve growth” and that inactivating Rb “can release the brake and coax nerve cells to grow much faster.” MH
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