We thank Dr. Baraka for his insightful comments on our article.1As Dr. Baraka pointed out, one of our findings is that the muscle-type nicotinic acetylcholine receptor, when expressed in Xenopus  oocytes, is desensitized by succinylcholine after an initial activation. Because we have not studied the neuromuscular junction with all its components, we cannot from this type of study fully investigate the mechanism of action by succinylcholine-induced neuromuscular block.

To the best of our knowledge, succinylcholine seems to cause neuromuscular blockade due to a prolonged depolarization of the endplates,2which might include both desensitization of the muscle nicotinic acetylcholine receptors and inactivation of voltage-gated sodium channels. In addition, we suggest that the low affinity of succinylcholine for the presynaptic α3β2 nicotinic acetylcholine receptor subtype explains the lack of tetanic and train-of-four fade during succinylcholine-induced neuromuscular block.1 

*Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden. malin.jonsson@karolinska.se

Jonsson M, Dabrowski M, Gurley DA, Larsson O, Johnson EC, Fredholm BB, Eriksson LI: Activation and inhibition of human muscular and neuronal nicotinic acetylcholine receptors by succinylcholine. Anesthesiology 2006; 104:724–33
Bowman WC: Neuromuscular block. Br J Pharmacol 2006;147 (Suppl 1):S277–86.