Vanishing Weakness and Persistent Cardiac Dysrhythmia: Are We Dealing with Andersen Tawil Syndrome?

P, Jhansi Rani; Yashodhara, P.; Sundarachary, N V; Veeramma, U; Elahi, Shaik Mansoor; Amalakanti, Sridhar; Lalitha, A V

doi:10.1007/s12098-014-1677-z

Indian J Pediatr

2015

DOI: 10.1007/s12098-014-1677-z

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Vanishing Weakness and Persistent Cardiac Dysrhythmia: Are We Dealing with Andersen Tawil Syndrome?

Jhansi Rani P

P. Yashodhara

N V Sundarachary

et al.

Abstract: Andersen Tawil Syndrome (ATS) is a very rare type of periodic paralysis; the authors present a case report from South India with features that have not been reported earlier. This case suggests many unexplored hypotheses for the disease and argues the need for physician sensitization of this entity.

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2016

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Functional up-regulation of Nav1.8 sodium channel on dorsal root ganglia neurons contributes to the induction of scorpion sting pain

Hua

Jiao

et al. 2016

ABBS

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BmK I, purified from the venom of scorpion Buthus martensi Karsch (BmK), is a receptor site-3-specific modulator of voltage-gated sodium channels (VGSCs) and can induce pain-related behaviors in rats. The tetrodotoxin-resistant (TTX-R) sodium channel Nav1.8 contributes to most of the sodium current underlying the action potential upstroke in dorsal root ganglia (DRG) neurons and may serve as a critical ion channel targeted by BmK I. Herein, using electrophysiological, molecular, and behavioral approaches, we investigated whether the aberrant expression of Nav1.8 in DRG contributes to generation of pain induced by BmK I. The expression of Nav1.8 was found to be significantly increased at both mRNA and protein levels following intraplantar injection of BmK I in rats. In addition, the current density of TTX-R Nav1.8 sodium channel is significantly increased and the gating kinetics of Nav1.8 is also altered in DRG neurons from BmK I-treated rats. Furthermore, spontaneous pain and mechanical allodynia, but not thermal hyperalgesia induced by BmK I, are significantly alleviated through either blockade of the Nav1.8 sodium channel by its selective blocker A-803467 or knockdown of the Nav1.8 expression in DRG by antisense oligodeoxynucleotide (AS-ODN) targeting Nav1.8 in rats. Finally, BmK I was shown to induce enhanced pain behaviors in complete freund's adjuvant (CFA)-inflamed rats, which was partly due to the over-expression of Nav1.8 in DRG. Our results suggest that functional up-regulation of Nav1.8 channel on DRG neurons contributes to the development of BmK I-induced pain in rats.

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Functional up-regulation of Nav1.8 sodium channel on dorsal root ganglia neurons contributes to the induction of scorpion sting pain

Hua

Jiao

et al. 2016

ABBS

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Vanishing Weakness and Persistent Cardiac Dysrhythmia: Are We Dealing with Andersen Tawil Syndrome?

Cited by 1 publication

References 10 publications

Functional up-regulation of Nav1.8 sodium channel on dorsal root ganglia neurons contributes to the induction of scorpion sting pain

Functional up-regulation of Nav1.8 sodium channel on dorsal root ganglia neurons contributes to the induction of scorpion sting pain

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