Experimental neurology
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Experimental neurology · May 2010
ReviewThe potentiation of peripheral nerve sheaths in regeneration and repair.
Traumatic injury to the nervous system often results in life changing loss of neurological function. Spontaneous neural regeneration occurs rarely and the outcome of therapeutic intervention is most often unacceptable. An intensive effort is underway to improve methods and technologies for nervous system repair. ⋯ Experimental alteration of nerve sheath composition can also potentiate nerve and improve key features of nerve regeneration. For instance, enzymatic degradation of inhibitory chondroitin sulfate proteoglycan mimics endogenous processes that potentiate degenerated nerve and improves the outcome of direct nerve repair and grafting in animal models. This review provides a perspective of the essential role that peripheral nerve sheaths play in regulating axonal regeneration and focuses on discoveries leading to the inception and development of novel therapies for nerve repair.
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Experimental neurology · May 2010
ReviewA conditioning lesion induces changes in gene expression and axonal transport that enhance regeneration by increasing the intrinsic growth state of axons.
Injury of axons in the peripheral nervous system (PNS) induces transcription-dependent changes in gene expression and axonal transport that promote effective regeneration by increasing the intrinsic growth state of axons. Regeneration is enhanced in axons re-injured 1-2 weeks after the intrinsic growth state has been increased by such a prior conditioning lesion (CL). The intrinsic growth state does not increase after axons are injured in the mammalian central nervous system (CNS), where they lack the capacity for effective regeneration. ⋯ A CL of peripheral branches increases the intrinsic growth state of central branches in the dorsal columns of the spinal cord, enabling these axons to undergo lengthy regeneration in a segment of peripheral nerve transplanted into the spinal cord (i.e., a peripheral nerve graft). This regeneration does not occur in the absence of a CL. We will examine how changes in gene expression and axonal transport induced by a CL may promote this regeneration.