No abstract

The use of vein or muscle grafts to bridge nerve defects longer than 1-1.5 cm gives poor results. Veins collapse and in muscle grafts axons may regrow outside the graft. We used veins (to guide regeneration) filled with muscle (to avoid vein collapse). Nerve regeneration through 1 and 2 cm grafts made of vein plus muscle was compared with similarly long traditional nerve grafts, free fresh muscle grafts, and empty vein grafts. Regeneration was assessed clinically and histologically (qualitative and quantitative evaluation) in the graft and distal nerve stumps. Vein plus muscle grafts were superior to vein and fresh muscle grafts both functionally and histologically. Functional results were similar to those found in traditional nerve grafts, but axon number was superior in the veins filled with muscle. This suggests that vein filled with muscle might serve as a grafting conduit for the repair of peripheral nerve injuries and could give better results than traditional nerve grafting.

No abstract

Acetylcholine is the main neurotransmitter at the mammalian neuromuscular junction (NMJ) where nicotinic acetylcholine receptors mediate the signaling between nerve terminals and muscle fibers. We show that under glutamatergic transmission, rat NMJ switches from cholinergic type synapse to glutamatergic synapse. Connecting skeletal muscle to the lateral white matter of the spinal cord by grafting the distal stump of the transected motor nerve produced functional muscle reinnervation. The restored neuromuscular activity became resistant to common curare blockers but sensitive to the glutamate ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist. Analysis of the regenerated nerve disclosed new glutamatergic axons and the disappearance of cholinergic fibers. Many axons belonged to the supraspinal neurons located in the red nucleus and the brainstem nuclei. Finally, the innervated muscle displayed high expression and clustering of ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunits glutamate receptors 1 and 2. Our data suggest that supraspinal neurons can target skeletal muscle, which retains the plasticity to generate functional glutamatergic NMJ.glutamate ͉ neuromuscular junction ͉ red nucleus T raumatic paraplegia caused by spinal cord injury is still an irreversible condition. So far, there is no medical or surgical treatment capable of curing paraplegia. The CNS is ''nonpermissive'' for the advancement of injured axons because of an abundance of growth-inhibitory molecules in the myelin and the glial scar (1-3). In addition, there are no growth-promoting factors at the neuronal growth cone or at the somata. However, when peripheral nerves (PN) are directly grafted into the CNS, central axons can progress throughout the peripheral endoneural tubes, suggesting they can regenerate in an appropriate environment (4-7). The central fibers that are diverted into a nerve graft implanted within a healthy structure derive from neurons axotomized during the grafting procedure and not from uninjured neurons spared by nerve graft implantation (8). Regrowth ceases as soon as axons contact the CNS milieu again. Various studies have demonstrated that central axons can elongate within autologous PN grafted into the spinal cord and form functional synapses with skeletal muscles, leading to motor and sensory recovery (7, 9-11). Spinal cord neurons, as well as the midbrain and brainstem neurons that originate the rubrospinal, vestibulospinal, and reticulospinal tracts, are endowed with a high capability of axonal regeneration into PN transplants (12-15). Thus, in an attempt to bypass a spinal cord lesion by connecting descending motor fibers with skeletal muscles, muscular nerve branches were inserted into the severed lateral bundle of monkey spinal cord (11). The new connection produced muscle reinnervation and restored motor function. This result raised the possibility that the regrowth of axons descending from central noncholinergic neurons and cut during the grafting procedure could be re...

The results of experimental research, as well as of a large clinical series (n = 51) of direct muscle neurotization, have been encouraging enough to warrant extending the indications for the procedure to patients in whom traditional repair by direct nerve suture or nerve graft is impossible, because of the lack of a distal nerve segment, or because of destruction of the neural portion of one or more muscle groups. Prerequisites include a satisfactory volume of muscle with sufficient vascularity and adequate postoperative joint and muscle immobilization.