Search results
Results From The WOW.Com Content Network
It is an enzyme that catalyzes the breakdown of acetylcholine and some other choline esters that function as neurotransmitters: acetylcholine + H 2 O = choline + acetate. It is found at mainly neuromuscular junctions and in chemical synapses of the cholinergic type, where its activity serves to terminate cholinergic synaptic transmission.
A cholinergic crisis is an over-stimulation at a neuromuscular junction due to an excess of acetylcholine, [1] as a result of the inactivity of the acetylcholinesterase enzyme, which normally breaks down acetylcholine.
The enzyme acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle ...
Acetylcholine Acetylcholinesterase Acetylcholinesterase inhibition. Acetylcholinesterase inhibitors (AChEIs) also often called cholinesterase inhibitors, [1] inhibit the enzyme acetylcholinesterase from breaking down the neurotransmitter acetylcholine into choline and acetate, [2] thereby increasing both the level and duration of action of acetylcholine in the central nervous system, autonomic ...
The hypothesis states that a possible cause of AD is the reduced synthesis of acetylcholine, a neurotransmitter involved in both memory and learning, two important components of AD. Many current drug therapies for AD are centered on the cholinergic hypothesis, although not all have been effective.
Acetylcholine (ACh) is an organic compound that functions in the brain and body of many types of animals (including humans) as a neurotransmitter. [1] Its name is derived from its chemical structure: it is an ester of acetic acid and choline. [2] Parts in the body that use or are affected by acetylcholine are referred to as cholinergic.
Choline acetyltransferase was first described by David Nachmansohn and A. L. Machado in 1943. [6] A German biochemist, Nachmansohn had been studying the process of nerve impulse conduction and utilization of energy-yielding chemical reactions in cells, expanding upon the works of Nobel laureates Otto Warburg and Otto Meyerhof on fermentation, glycolysis, and muscle contraction.
This causes repetitive excitation that lasts longer than a normal acetylcholine excitation and is most likely explained by the resistance of depolarizing agents to the enzyme acetylcholinesterase. The constant depolarization and triggering of the receptors keeps the endplate resistant to activation by acetylcholine.