If AchE is present in the synaptic cleft, then how is it possible for Ach to travel upto the T-tubules and Ach receptors? or is the AchE inhibited during muscle contraction? If so, what inhibits/activates the AchE back?
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Solution
Excess ACh is always broken by the AChE when the receptors receive sufficient ACh. The enzymes are not inhibited, the breaking is based on the requirement.