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July 1, 1993The Journal of PhysiologyOpen Access

Loss of Na+ channel inactivation by anemone toxin (ATX II) mimics the myotonic state in hyperkalaemic periodic paralysis.

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Population

Rat skeletal muscle (blebs of surface membrane from mechanically disrupted fibres)

Comparison

Anemone toxin (ATX II) up to 10 microM vs Baseline/untreated state (0 microM ATX II)

Design

Preclinical

Authors

SCStephen C. CannonBoston UniversityDCDavid P. CoreyHarvard University

Discussion

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Implication

Supports sodium channel loss-of-inactivation as sufficient for myotonia in rodents; leaves open human translation and therapeutic relevance.

Structured PICO

P
Population
Rat skeletal muscle (blebs of surface membrane from mechanically disrupted fibres)
I
Intervention
Anemone toxin (ATX II) up to 10 microM
C
Comparator
Baseline/untreated state (0 microM ATX II)
O
Outcome
Single-channel sodium currents and relaxation of tension after a single twitchsurrogate

Loss of sodium channel inactivation by ATX II in rat skeletal muscle is sufficient to produce the electrical and mechanical features of myotonia, demonstrating that only a small proportion of abnormal channels is needed.

Cite This Study

Cannon et al. (1993) studied this question.

synapsesocial.com/papers/6a70a2f0ac440176ef294d98https://doi.org/10.1113/jphysiol.1993.sp019731
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Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Cable parameters, sodium, potassium, chloride, and water content, and potassium efflux in isolated external intercostal muscle of normal volunteers and patients with myotonia congenita1971 · 158 citations
  2. 2Kinetic properties of single sodium channels in rat heart and rat brain.1989 · 90 citations
  3. 3The effects of <i>Anemonia sulcata</i> toxin II on vertebrate skeletal muscle1985 · 7 citations
  4. 4Hyperkalemic Periodic Paralysis and the Adult Muscle Sodium Channel α-Subunit Gene1990 · 306 citations