Effect of Methylcobalamin on Voltage-Gated Sodium Channels (Vgscs) Expression in Neuropathic Painanimal Model

Endang Mutiawati^1,2* , K.R.T. Lucas Meliala³, Ginus Partadiredja⁴, Dhirgo Adji⁵ and Raden Wasito⁵  

¹Department of Neurology, School of Medicine, Universitas Syiah Kuala, Banda Aceh, Indonesia

²Department of Neurology, Dr. Zainoel Abidin Hospital, Banda Aceh, Indonesia

³Department of Neurology, Faculty of Medicine, Gadjah Mada University, Yogyakarta, Indonesia

⁴Department of Physiology, Faculty of Medicine, Gadjah Mada University, Yogyakarta, Indonesia

⁵Department of Pathology, Faculty of Veterinary Medicine, Universitas Gadjah Mada, Yogyakarta, Indonesia

Corresponding Author E-mail: endangmutiawati@unsyiah.ac.id

Abstract:

The objective of this study wasto assess the effect of methylcobalaminonmechanical allodynia and the voltage-gated sodium channels (VGSCs) expression of injured nerves in spinal nerve ligation-induced neuropathic pain model in animals.Three different doses of methylcobalamin were administrated intramuscularly into neuropathic pain rat model, twice a week for 14 weeks. The effect of methylcobalamin on neuropathic pain was assessed using mechanical allodynia (using the von Frey filaments) while its effect on VGSC expression was assessed using immunohistochemistry. ANOVA and independent t-test were employed to compared the effect of methylcobalamin on mechanical allodynia between groups.The size of von Frey filament that induced the first onset of mechanical allodynia was smaller in control group compared to 50µg methylcobalamin group (p=0.013) and methylcobalamin 100µg group (p=0.019). There is a dose–response relationship between methylcobalamin dose and the average duration of mechanical allodynia (43.8, 38.2, 30.6 and 29.6 days for control, 50µg, 100µg, and 150µg methylcobalamin group, respectively) with a significant different observed between control and 150µg methylcobalamin group only (p=0.027). Nerve tissues from all animals within control group expressed VGSC while all nerve tissues from both 100µg, and 150µg methylcobalamin, had no VGCS expression. In conclusion, methylcobalamin is potentially shorten the duration of mechanical allodynia and increase pain threshold in neuropathic pain animal model. These effects might associate with reduction of VGSC expression on the injured neurons.

Keywords: Neuropathic pain; Methylcobalamin; Pathology; Sodium ion channel

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