MORPHOLOGICAL ABNORMALITIES IN MYELINATED NERVE FIBRES CAUSED BY LEIURUS, CENTRUROIDES AND PHONEUTRIA VENOMS AND THEIR PREVENTION BY TETRODOTOXIN

Abstract

SUMMARYMorphological changes in peripheral nerve caused by the venoms of the scorpions Leiurus quinquestriatus and Centruroides sculpturatus were compared with those caused by Phoneutria nigriventer spider venom. Both scorpion venoms are known to delay the inactivation of sodium currents, Centruroides venom also altering the voltage dependence of sodium gating. Venom was injected by means of a glass micropipette into the sciatic nerves of anaesthetized mice. After survival times ranging from 15 min to 24 h the nerves were examined by light and electron microscopy. The two scorpion venoms caused alterations virtually identical to those produced by Phoneutria venom, which included swelling of the nodal axoplasm and accumulation of fluid in the periaxonal space of myelinated fibres. These alterations were most marked after 1 to 2 h and had largely disappeared by 24 h. Pre-treatment of the nerves with tetrodotoxin, which specifically blocks sodium channels, completely prevented both the nodal axoplasmic swelling and the periaxonal oedema. It seems likely that these effects result from an action common to the three venoms and that this is probably a delay in the inactivation of sodium current at the node of Ranvier.

Effects of hemodialysis on intraneural blood flow in end‐stage kidney disease

“…Previous studies using nerve excitability measures in ESKD demonstrated a pattern consistent with axonal membrane depolarization, with changes correlating strongly with potassium concentration . Membrane depolarization due to chronic hyperkalaemia may result in nerve enlargement secondary to swelling of the node of Ranvier and myelin sheath as well as expansion of the periaxonal space . Of note, the present study demonstrated significant correlation between INBF and nerve excitability values, suggesting a close interaction between electrolyte imbalance, impaired nerve function and altered nerve morphology and blood flow.…”

Blockade of acetylcholine release at the motor endplate by a polypeptide from the venom of Phoneutria nigriventer

“…These effects were attributed to activation of voltage-dependent sodium channels in both nerve and muscle fibres (Fontana & Vital-Brasil, 1985). Morphological changes produced by the venom in peripheral nerves of mice were also reported (Cruz-Hofling et al, 1985;Love et al, 1986).…”

Diabetic Peripheral Neuropathy: Should a Chaperone Accompany Our Therapeutic Approach?

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