Snake venom three finger toxins (3FTxs) are a non-enzymatic family of venom proteins abundantly found in elapids. We have purified a 7579.5 ± 0.591 Da 3FTx named as Nk-3FTx from the venom of Naja kaouthia of North East India origin. The primary structure was determined by a combination of N-terminal sequencing and electrospray ionization liquid chromatography-mass spectrometry/mass spectrometry. Biochemical and biological characterization reveal that it is nontoxic to human cell lines and exhibit mild anticoagulant activity when tested on citrated human plasma. Nk-3FTx was found to affect the compound action potential (CAP) and nerve conduction velocity of isolated toad sciatic nerve. This is the first report of a non-conventional 3FTx from Naja kaouthia venom that reduces CAP for its neurotoxic effect. Further studies can be carried out to understand the mechanism of action and to explore its potential therapeutic application.

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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.

Demyelination in peripheral nerves causes dysfunction of slowing down and stoppage of nerve impulses causing many neurological diseases, such as chronic inflammatory demyelinating polyneuropathy, Guillain-Barre syndrome, etc. This paper aims to develop a recovery model having interaction of a demyelinated nerve with a normal myelinated nerve. We validated the model by coupling between peripheral nerve of toad (demyelinated with Naja kaouthia venom) and a normal nerve of toad. An increase in both nerve conduction velocity as well as compound action potential amplitude is observed in the repetition of the experiments indicating gradual recovery of the patients. The significance behind this work is to suppress the malfunctioning of the demyelinated nerve by the normal electro-physiological activity of the normal nerve for speedy recovery using coupling model. The recovery model will be used in the treatment of neurological disorders with the influence of normal neuro physiological properties of a normal adjacent nerve.