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The Effect of Methylcobalamin on Regeneration of Motor End Plate with Injured Peripheral Nerves

Author: WenRui
Tutor: ZuoSuYun
School: Henan University
Course: Human Anatomy,Histology and Embryology
Keywords: Mecobalamin Nerve injury Motor end plate Acetylcholine receptor Acetylcholinesterase
CLC: R96
Type: Master's thesis
Year: 2010
Downloads: 95
Quote: 1
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Abstract

Skeletal muscle function recovery after peripheral nerve injury has been a hot topic in the field of neuroscience. The skeletal muscle is the target organ of the peripheral nervous system, skeletal muscle to maintain normal function depends on Nerves and regulation. After peripheral nerve injury, skeletal muscle if not timely get reinnervation irreversible atrophy and even loss of function. Somatic motor nerve endings, morphology is often called the motor end plate (motor end plat, MEP), physiology, also known as neuromuscular junction (neuromuscular junction, NMJ) is present in skeletal muscle and nerve fibers between specialized area. Regeneration and repair of nerve function should ultimately rely on the regeneration and reconstruction of the motor endplate, functional status reflects the functional state of the muscle endplate. In recent years, done a lot of research on peripheral nerve injury, although progress has been made, but the recovery of neurological function is still unsatisfactory. Studies have found that: methylcobalamin can promote the main component of myelin - the synthesis of lecithin and can participate in the neurotransmitter acetylcholine (ACh) synthesis of acetylcholine to promote axoplasmic transport and axonal regeneration in the treatment of peripheral neuropathy, especially diabetic efficacy has been confirmed in animal experiments and clinical, but its recovery after nerve injury in skeletal muscle and its motor end plate regeneration effect and mechanism of reported less movement after nerve injury, especially mecobalamin endplate acetylcholinesterase (acetylcholinesterase, AChE), acetylcholine receptor (acetylcholine receptor, AChR) changes reported less. Therefore, this experiment rat sciatic nerve injury model the local injection mecobalamin, observe different time neurophysiological, muscle wet weight motor endplate morphology, acetylcholinesterase, acetylcholine receptor changes to explore mecobalamin nerve injury After the motor endplate role in promoting recovery, and provide a theoretical basis for clinical treatment of neurological disorders. METHODS: The experiment selected adult male Wistar rats (250-300g) 90 rats were randomly divided into group A (Methylcobalamin group), B (saline control group) two groups of 45. Prepared by clamping the rat sciatic nerve nerve injury model, about 2-3 hours after recovery of animal consciousness, local injection of drugs. Group A daily injection of a cobalamin 400 ul / kg, group B daily injections of normal saline. 1, 4 and 8 weeks after surgery were randomly selected A, B rats of the 15 measured nerve conduction velocity to evaluate nerve function, and then complete dissecting gastrocnemius weighed called wet weight. Take muscle tissue were performed gold chloride staining, light microscope observation of the motor endplate changes; The AChE enzyme histochemical staining of AChE content, combined with image analysis system densitometry; the AChR fluorescent staining acetylcholine receptor changes ; statistical analysis of all the data rows. Results: 1, after 1 week all rats ipsilateral foot ulcers, difficult to stand. Nerve conduction velocity is reduced, compared to the two groups was not statistically significant (P gt; 0.05) Two sets of gastrocnemius muscle wet weight was not statistically significant (P gt; 0.05). The two sets of microscopic motor end plate degeneration, reduce the axon terminal branches. The AChE staining: AChE content decreased, the two sets of optical density analysis was not statistically significant (P gt; 0.05). Two sets of acetylcholine receptor incomplete form, reduce wrinkles. 2 and 4 weeks after the rats in group A than in group B improved significantly in group B, walking gait uncoordinated. Group A than in group B nerve conduction velocity has been restored, the two groups was statistically significant (P lt; 0.05) Gastrocnemius wet weight of the two groups was statistically significant (P lt; 0.05) Group A motor endplate increase in the number of deeply stained, irregular. No significant increase in the number of group B motor end plate, light staining, irregular shaped form. The AChE staining: two groups of AChE positive optical density analysis was statistically significant (P lt; 0.05). Two groups of acetylcholine receptor increase in the number of group A form tends to complete the form of the B group is still not rule. 3, 8 weeks after surgery rats in group A wound has healed, gait coordination. Walking on Group B is still skewed. Nerve conduction velocity in group A than in group B was significantly restored the two groups was statistically significant (P lt; 0.01). A group and B group gastrocnemius wet weight statistically significant difference (P lt; 0.01). Group A motor endplate morphology and coloration close to normal in group B did not change significantly. The AChE staining: A group of AChE activity was significantly higher than that in group B, two sets of positive area optical density analysis were significantly different (P lt; 0.01). A group of acetylcholine receptor form mature B group is still not rule. Conclusion: 1, methylcobalamin can delay degeneration of peripheral nerve injury after motor end plate, and promote regeneration of motor end plate; 2, mecobalamin delay after nerve injury in skeletal muscle wet weight decreased, thus delaying the occurrence of skeletal muscle atrophy; Methylcobalamin can improve the motor end plate acetylcholinesterase and mature content of the acetylcholine receptor, to promote the role of the motor end plate after peripheral nerve injury repair; 4, methylcobalamin can speed up the nerve injury nerve conduction recovery.

The Effect of Methylcobalamin on Regeneration of Motor End Plate with Injured Peripheral Nerves

Abstract

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