Abstract:

Neurons in the central nervous system (CNS) of adult mammals have a weak intrinsic regenerative capacity, which is one contributing factor to the failure of axonal regeneration. Finding the means to elevate the regenerative capacity of axotomised neurons is one requirement for successful regeneration. Forty-five years ago, it was reported that crushing of the sciatic nerves of adult mice two weeks before cutting the nerves accelerated the regrowth of their axons (McQuarrie and . The nerve injury two weeks before triggered the regeneration machinery in the injured neurons, leading to faster axonal regrowth after a subsequent lesion. Later it was found that a lesion to a peripheral nerve also strongly enhanced the regeneration of the central branches of the appropriate primary sensory neurons . This phenomenon is termed preconditioning lesion (or conditioning lesion if the central branches of the sensory neurons are injured after a concomitant injury to their peripheral branches). Conditioning lesion of peripheral nerves has been used in combination with other strategies in promoting sensory axon regeneration in injured spinal cord in animal models. Although conditioning lesion cannot be translated into clinical practice as intentional injury to the peripheral nerves of the patients would be counterproductive, studying the underlying molecular events will reveal how neurons respond to axonal injuries, leading to the development of practical therapeutic strategies for axonal regeneration.