Major ANS(Autonomic Nervous System) Neurotransmitters

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Chapter: Anatomy and Physiology for Health Professionals: Autonomic Nervous System (ANS)

The major ANS neurotransmitters are ACh and NE. ACh is secreted by somatic motor neurons as well, but in the ANS, it is released by all preganglionic axons and all parasympathetic postganglionic axons at synapses with their effectors.


Major ANS Neurotransmitters

The major ANS neurotransmitters are ACh and NE. ACh is secreted by somatic motor neurons as well, but in the ANS, it is released by all preganglionic axons and all parasympathetic postganglionic axons at synapses with their effectors. The cholinergic fibers release ACh. Most sympathetic postganglionic axons or adrenergic fibers release NE. One exception is sympathetic postgangli-onic fibers, which secrete ACh onto the sweat glands.

There are no consistent excitatory or inhibitory effects of ACh or NE upon their effectors. This is because the action of each neurotransmitter is based on the receptor to which it binds. Each ANS neu-rotransmitter binds with two or more types of recep-tors. In this way, the neurotransmitter can activate or inhibit actions at various body targets.

Actions of Autonomic Neurotransmitters

Autonomic neurotransmitters exert their actions by binding to protein receptors in the effector cell mem-branes, such as by stimulation at neuromuscular ­junctions and synapses. The effector cell ­membranes are altered by receptor binding. Permeability to cer-tain ions can increase. In smooth muscle cells, action potentials may occur, followed by muscular contrac-tion. Also, gland cells may respond to membrane changes by secreting various products.

Termination of Autonomic Neurotransmitter Actions

Acetylcholinesterase (AChE) is the enzyme that quickly decomposes ACh released by cholinergic fibers. This decomposition also occurs at neuromus-cular junctions in the skeletal muscle. Therefore, ACh commonly affects postsynaptic membranes for only fractions of a second. NE released from adrener-gic fibers is mostly removed from synapses by active transport back into nerve endings. Monoamine oxi-dase is the mitochondrial enzyme that inactivates NE, usually within a few seconds. Some NE molecules can diffuse to nearby tissues or the bloodstream to be decomposed by other enzymes. Other NE molecules stay active for some time. Therefore, NE is able to produce a longer effect than ACh. When the adrenal medulla releases NE and epinephrine into the blood circulation, triggered by sympathetic stimulation, the substances can cause sympathetic responses in organs that may last up to 20 minutes.

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