Quantifying Demyelination in NK venom treated nerve using its electric circuit model.

H K Das,P P Sahu,R Doley,D Das

doi:10.1038/srep22385

H K Das, P P Sahu + Show 2 more

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https://doi.org/10.1038/srep22385

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Journal: Scientific Reports	Publication Date: Mar 2, 2016
Citations: 5	License type: CC BY 4.0

Affiliation: Tezpur University

Abstract

Reduction of myelin in peripheral nerve causes critical demyelinating diseases such as chronic inflammatory demyelinating polyneuropathy, Guillain-Barre syndrome, etc. Clinical monitoring of these diseases requires rapid and non-invasive quantification of demyelination. Here we have developed formulation of nerve conduction velocity (NCV) in terms of demyelination considering electric circuit model of a nerve having bundle of axons for its quantification from NCV measurements. This approach has been validated and demonstrated with toad nerve model treated with crude Naja kaouthia (NK) venom and also shows the effect of Phospholipase A2 and three finger neurotoxin from NK-venom on peripheral nerve. This opens future scope for non-invasive clinical measurement of demyelination.

Highlights

Speedy and efficient transmission of action potential sequences carrying neuro-signals depends on axon membrane sheath made by myelin[1,2]
The nerve conduction signals obtained from proximal and distal action potential nerve treated with 0.1 μg/ml, 1.0 μg/ml and 10 μg/ml crude venom concentration shows reduction of nerve conduction velocity (NCV) due to demyelination of axons in the nerve (Fig. 2)
We have performed experiments on sciatic nerve isolated from toad our findings may open a non-invasive clinical way to quantify demyelination of a peripheral nerve from NCV measurements

Summary

Introduction

Speedy and efficient transmission of action potential sequences carrying neuro-signals depends on axon membrane sheath made by myelin[1,2]. Node of Ranvier (NoR) is distorted by demyelination leading to slow movement of Na+/K+ ions Clinical analysis of these diseases requires quantification of demyelination. In this direction, invasive measurement of demyelin/myelin thickness using SEM imaging and nerve biopsy is a destructive and clinically critical and harmful for the patients. Previous studies show that PLA2 causes Alzheimer’s disease[18], Multiple Scelerosis (MS)[19,20], Epilepsy[21] due to motor dysfunction In this direction the development of toad nerve model has revolutionized the field of neuroscience especially for human peripheral clinical treatment[22,23]. NCV is formulated by using electric circuit model of a nerve having bundle of axons misali egxnpeedrbimy eanlitganlmpoeinnttfsaocftobrl,aAck=do2t1s

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