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The mechanism formally parallels the -elimination reaction catalyzed by PLP-dependant enzymes which accept cysteine thioethers as substrates and likely play a role in the renal toxicity and carcinogenicity of halogen-alkenes through their urinary metabolites [125]
administration, resulting in flaccid paralysis (Renew, 2026) Succinylcholine's effect during Phase I block is purely postsynaptic and results from a relatively constant reduction in twitch amplitude caused by the prolonged occupancy of postsynaptic nAChRs by succinylcholine, which interferes with the normal acetylcholine-mediated neurotransmission when a motoneuron is stimulated (Figure 2)(Jonsson et al, 2006) Clinically: Equal reduction in all four twitches during train-of-four stimulation No fade pattern observed Phase II Block (Presynaptic & Open Channel Mechanisms) Occurs with abnormally high doses or repeated administration : Phase I block progresses to a state resembling non-depolarizing blockade Characterized by: Presynaptic autoreceptor antagonism Succinylcholine has been shown to antagonize neuronal 32 nACh receptors with an IC50 that is ~10-times higher than its EC50 for stimulating the muscle-type (11) nACh receptors (Freeman, 1968
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