A novel chronic nerve compression model in the rat

Current animal models of chronic peripheral nerve compression are mainly silicone tube models. However, the cross section of the rat sciatic nerve is not a perfect circle, and there are differences in the diameter of the sciatic nerve due to individual differences. The use of a silicone tube with a uniform internal diameter may not provide a reliable and consistent model. We have established a chronic sciatic nerve compression model that can induce demyelination of the sciatic nerve and lead to atrophy of skeletal muscle. In 3-week-old pups and adult rats, the sciatic nerve of the right hind limb was exposed, and a piece of surgical latex glove was gently placed under the nerve. N-butyl-cyanoacrylate was then placed over the nerve, and after it had set, another piece of glove latex was placed on top of the target area and allowed to adhere to the first piece to form a sandwich-like complex. Thus, a chronic sciatic nerve compression model was produced. Control pups with latex or N-butyl-cyanoacrylate were also prepared. Functional changes to nerves were assessed using the hot plate test and electromyography. Immunofluorescence and electron microscopy analyses of the nerves were performed to quantify the degree of neuropathological change. Masson staining was conducted to assess the degree of fibrosis in the gastrocnemius and intrinsic paw muscles. The pup group rats subjected to nerve compression displayed thermal hypoesthesia and a gradual decrease in nerve conduction velocity at 2 weeks after surgery. Neuropathological studies demonstrated that the model caused nerve demyelination and axonal irregularities and triggered collagen deposition in the epineurium and perineurium of the affected nerve at 8 weeks after surgery. The degree of fibrosis in the gastrocnemius and intrinsic paw muscles was significantly increased at 20 weeks after surgery. In conclusion, our novel model can reproduce the functional and histological changes of chronic nerve compression injury that occurs in humans and it will be a useful new tool for investigating the mechanisms underlying chronic nerve compression.

Brain remodeling after chronic median nerve compression in a rat model

Carpal tunnel syndrome is the most common compressive neuropathy,presenting with sensorimotor dysfunction.In carpal tunnel syndrome patients,irregular afferent signals on functional magnetic resonance imaging are associated with changes in neural plasticity during peripheral nerve injury.However,it is difficult to obtain multi-point neuroimaging data of the brain in the clinic.In the present study,a rat model of median nerve compression was established by median nerve ligation,i.e.,carpal tunnel syndrome model.Sensory cortex remodeling was determined by functional magnetic resonance imaging between normal rats and carpal tunnel syndrome models at 2 weeks and 2 months after operation.Stimulation of bilateral paws by electricity for 30 seconds,alternating with 30 seconds of rest period（repeatedly 3 times）,resulted in activation of the contralateral sensorimotor cortex in normal rats.When carpal tunnel syndrome rats received this stimulation,the contralateral cerebral hemisphere was markedly activated at 2 weeks after operation,including the primary motor cortex,cerebellum,and thalamus.Moreover,this activation was not visible at 2 months after operation.These findings suggest that significant remodeling of the cerebral cortex appears at 2 weeks and 2 months after median nerve compression.