In Vitro Neuromuscular Blockade Caused by Micrurus surinamensis Venom

Coral snakes are the American representatives of the Elapidae family. Micrurus surinamensis stands out as the largest coral snake species found in Brazil, notable for its semiaquatic habits and a diet consisting exclusively of fish. Its venom is primarily made up of three-finger toxins (3FTx), while the presence of phospholipases A₂ (PLA₂) appears to be inconsistent across different studies.

Methods:
This study investigated the neuromuscular effects of M. surinamensis venom using isolated neuromuscular models: the mouse phrenic nerve–diaphragm (PND) and chick biventer cervicis (BC) models. Mouse sciatic nerve preparations were also used.

Results:
The venom-induced neuromuscular blockade occurred in both the PND and BC preparations in a concentration- and time-dependent fashion, with the BC model demonstrating greater sensitivity. In the PND model, the findings included the following: the concentration- and time-dependent inhibition of tetanic contractions, without evidence of a tetanic fade; the full recovery of neuromuscular function following washing; reduced muscle depolarization induced by carbachol; and the suppression of miniature endplate potentials. In the BC preparation, the venom abolished contractile responses to both acetylcholine and carbachol, and washing led to partial recovery from the neuromuscular blockade. In both models, the partial and temporary restoration of neuromuscular function was achieved using neostigmine or 3,4-diaminopyridine. The compound action potentials in the mouse sciatic nerve remained unaffected. Additionally, no signs of myotoxicity were detected in either the PND or BC preparations, as evidenced bya stable muscle tension baseline; a preserved response to direct muscle stimulation; an unchanged muscle resting membrane potential in the PND model; an unaltered contractile response to exogenous potassium in the BC model; and the absence of histological damage in the muscle tissue. The venom showed no PLA₂ enzymatic activity.

Conclusion:
These findings support the conclusion that the neuromuscular blockade caused by M. surinamensis venom is predominantly due to α-neurotoxins, probably of the 3FTx class. There was no contribution from β-neurotoxins (such as PLA₂) or significant muscle tissue injury .