By Albert E Pohland; Vulus R Dowell; J L Richard; Richard J Cole; Milven W Eklund; All authors
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Additional info for Microbial Toxins in Foods and Feeds : Cellular and Molecular Modes of Action
Sample text
The toxin might act as a mechanical blocker of the membrane channel through which acetylcholine moves. The other is that the toxin prevents exocytosis of acetylcholine from vesicles. Observations of the normal situation show that nerve stimulation is followed by migration and attachment to the inner or intracellular surface of the synaptic membrane by acetylcholine containing vesicles. Following this attachment the vesicles exocytose and the released acetylcholine moves across the membrane in channels abuting the surface of the vesicles to be released into the synaptic gap.
Under our conditions of experimentation with massive doses of toxin the maximum decrease before spontaneous recovery was 70 percent for the mouse and rat and 75 percent for the dog. Apart from the automaticity of heart muscle cell pulsation what does this mean about the role of acetylcholine neurotransmitter relative to noncholinergic nerve cells in heart physiology? Obviously for the cardiologist the toxin's cardiac effect raises anatomic-physiological questions about innervation of the heart and provides a tool for exploration of answers.
Whether toxin prevents exocytosis by masking a trigger or blocks channel translocation of acetylcholine either process can be nonenzymatic. Toxin may frustrate an enzymatic event such as exocytosis without itself acting as an enzyme. Enzyme inhibitors can be nonenzymatic. The nonenzymic aspect of the pipe and valve hypothesis satisfies the rule of Ockham's razor, namely, that entities should not be multiplied unnecessarily. Vesicle exocytosis follows stimulation. Upon stimulation, to repeat, the vesicle attaches to a specific site on the synaptic membrane, and only then does exocytosis follow.