Membrane continued interaction with excitable

Succinylcholine, similar to acetylcholine, interacts with the cholinergic receptors at the end plate region of the muscle, resulting in depolarization of the chemically excitable membrane. This, in turn, creates local action potentials, spreading them to and depolarizing the adjacent excitable membranes, finally culminating in a muscle contraction, or fasciculation, which is an uncoordinated muscle contraction. However, unlike acetylcholine, succinylcholine is not metabolized by acetylcholinesterase, and hence causes persistent depolarization of the end plate. The continuous presence of succinylcholine leads to inexcitability of the membrane adjacent to the end plate, resulting in... 

Once the neurotransmitter substance has interacted with the receptor sites on the postsynaptic membrane it must be deactivated so that it does not continuously excite or inhibit the membrane. There are at least three deactivation processes—mass transport away from the synaptic gap, reuptake, and enzymic degradation. 

Photosystem II reaction center is susceptible to light induced damage and steady state photosynthesis is maintained by continual repair of the photo-inactivated photosystems. An increase in the rate of inactivation (by over excitation of PS II) or a decrease in the rate of repair of PSII centers can result in accumulation of damaged PS II and consequent photoinhibition of photosynthesis. Since the assembly and stability of PS II complex involves close interaction with membrane lipids, photoinhibition and recovery of PS II centers are likely to be affected by the lipid composition of the thylakoid membrane. 

The function of the enzyme is rapidly and efficiently to catalyze the hydrolysis of ACh (Eq. 8.2). The significance of rapid destruction of ACh is to deactivate the neurotransmitter after it binds to the receptors so as not to accumulate to levels that produce a continuous barrage of impulses by repetitive interactions. After all, the depolarization produced by the ACh-receptor binding must be terminated so that the excitability of the postsynaptic membrane and its permeability can be restored by repolarization. Inhibition of AChE levels would then exist in the vicinity of effector cells. Extreme inhibition, such as may occur following irreversible blockade of the enzyme, would lead to cholinergic intoxication with fatal results. 

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