Cholinergic synapse mechanisms

The primary mechanism used by cholinergic synapses is enzymatic degradation. Acetylcholinesterase hydrolyzes acetylcholine to its components choline and acetate it is one of the fastest acting enzymes in the body and acetylcholine removal occurs in less than 1 msec. The most important mechanism for removal of norepinephrine from the neuroeffector junction is the reuptake of this neurotransmitter into the sympathetic neuron that released it. Norepinephrine may then be metabolized intraneuronally by monoamine oxidase (MAO). The circulating catecholamines — epinephrine and norepinephrine — are inactivated by catechol-O-methyltransferase (COMT) in the liver. 

Mechanism of Action A cholinesterase inhibitor that inhibits the enzyme acetylcholinesterase, thus increasing the concentration of acetylcholine at cholinergic synapses and enhancing cholinergic function in the CNS. Therapeutic Effect Slows the progression of Alzheimer s disease. 

Mechanism of Action A parasympathetic, anticholinesterase agent that inhibits destruction of acetylcholine by acetylcholinesterase, thus causing accumulation of acetylcholine at cholinergic synapses. Results in an increase in cholinergic responses such as miosis, increased tonus of intestinal and skeletal muscles, bronchial and ureteral constriction, bradycardia, and increased salivary and sweat gland secretions. Therapeutic Effect Diagnosis of myasthenia gravis. 

Acetylcholine is the endogenous neurotransmitter at cholinergic synapses and neuroeffector junctions in the central and peripheral nervous systems. The actions of acetylcholine are mediated through nicotinic and muscarinic cholinergic receptors, which transduce signals via distinct mechanisms. 

The reaction is the mechanism by which acetylcholine is made for neurotransmission in the axonal terminal bulbs of the cholinergic synapse. 

The toxicodynamics (mechanism of action) of OP are known the action is based on apparently irreversible acetylcholinesterase (AChE, EC 3.1.1.7) inhibition at the cholinergic synapses. The resulting accumulation... 

The level of AChE in the presynaptic and postsynaptic element is not in itself a decisive criterion of cholinergic transmission. A high content of AChE has been observed in many non-cholinergic neurons (see Hebb in ref. 16). On the other hand, cholinergic synapses have been described where no cholinesterases are detectable and the cessation of the ACh action is ensured by other mechanisms (see also Saccharov and Turpaev, ref. 18). 

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