acetylcholine

Examples of acetylcholine in the following topics:

• Cholinergic Neurons and Receptors

  • Acetylcholine is also the principal neurotransmitter in all autonomic ganglia.
  • Acetylcholine was first identified in 1914 by Henry Hallett Dale for its actions on heart tissue.
  • Acetylcholine was also the first neurotransmitter to be identified.
  • When acetylcholine binds to acetylcholine receptors on skeletal muscle fibers, it opens ligand-gated sodium channels in the cell membrane.
  • This human M2 muscarinic acetylcholine receptor is bound to an antagonist (ACh).

• Agonists, Antagonists, and Drugs

  • Blocking, hindering, or mimicking the action of acetylcholine has many uses in medicine.
  • Atropine's pharmacological effects are due to its ability to bind to muscarinic acetylcholine receptors.
  • A nicotinic agonist is a drug that mimics, in one way or another, the action of acetylcholine (ACh) at nicotinic acetylcholine receptors (nAChRs).
  • They are ligand-gated ion channels with binding sites for acetylcholine as well as other agonists.
  • In 2009 there were at least five drugs on the market that affect the nicotinic acetylcholine receptors.

• Peripheral Motor Endings

  • In vertebrates, the signal passes through the neuromuscular junction via the neurotransmitter acetylcholine.
  • Acetylcholine diffuses into the synaptic cleft and binds to the nicotinic acetylcholine receptors located on the motor end plate.
  • This blockage of acetylcholine receptors causes muscle weakness, often first exhibiting drooping eyelids and expanding to include overall muscle weakness and fatigue.
  • The binding of acetylcholine at the motor end plate leads to intracellular calcium release and interactions between myofibrils to elicit contraction.
  • Detailed view of a neuromuscular junction: 1) Presynaptic terminal; 2) Sarcolemma; 3) Synaptic vesicle; 4) Nicotinic acetylcholine receptor; 5) Mitochondrion.

• Paralysis-Causing Bacterial Neurotoxins

  • Botulinum toxin is a protein and neurotoxin, which blocks neuromuscular transmission through decreased acetylcholine release.
  • In 1949, Arnold Burgen's group discovered, through an elegant experiment, that botulinum toxin blocks neuromuscular transmission through decreased acetylcholine release.
  • This light chain is an enzyme (a protease) that attacks one of the fusion proteins (SNAP-25, syntaxin or synaptobrevin) at a neuromuscular junction, preventing vesicles from anchoring to the membrane to release acetylcholine.
  • By inhibiting acetylcholine release, the toxin interferes with nerve impulses and causes flaccid (sagging) paralysis of muscles in botulism, as opposed to the spastic paralysis seen in tetanus.
  • The SNAP-25 protein is required for vesicle fusion that releases neurotransmitters from the axon endings (in particular acetylcholine).

• Parasympathetic Responses

  • The parasympathetic nervous system uses chiefly acetylcholine (ACh) as its neurotransmitter, although peptides (such as cholecystokinin) may act on the PSNS as neurotransmitters.
  • Two different subtypes of nicotinic acetylcholine receptors with alpha and beta subunits are shown.
  • The acetylcholine binding sites are indicated by ACh.

• Types of Neurotransmitters by Function

  • The major types of neurotransmitters include acetylcholine, biogenic amines, and amino acids.  
  • Acetylcholine, which acts on the neuromuscular junction, was the first neurotransmitter identified.
  • Once released, acetylcholine binds to post-synaptic receptors and is degraded by acetylcholinesterase.
  • Acetylcholine-releasing neurons are also found in the central nervous system (CNS).

• Neurotransmitters

  • The cholinergic system is a neurotransmitter system of its own, and is based on the neurotransmitter acetylcholine (ACh).
  • Both of these receptors are named for chemicals that interact with the receptor in addition to the neurotransmitter acetylcholine.
  • Nicotine, the chemical in tobacco, binds to the nicotinic receptor and activates it similarly to acetylcholine.
  • When acetylcholine binds to the nicotinic receptor, the postsynaptic cell is depolarized.
  • However, when acetylcholine binds to the muscarinic receptor, it might cause depolarization or hyperpolarization of the target cell.

• Function and Physiology of the Spinal Nerves

  • Nerves that release acetylcholine are said to be cholinergic.
  • In the parasympathetic system, ganglionic neurons use acetylcholine as a neurotransmitter to stimulate muscarinic receptors.
  • Instead the presynaptic neuron releases acetylcholine to act on nicotinic receptors.
  • Upper motor neurons release acetylcholine.
  • Acetylcholine is released from the axon terminal knobs of alpha motor neurons and received by postsynaptic receptors (nicotinic acetylcholine receptors) of muscles, thereby relaying the stimulus to contract muscle fibers.

• Postganglionic Neurons

  • In the parasympathetic division, they are cholinergic and use acetylcholine as their neurotransmitter.
  • At the synapses within the ganglia, the preganglionic neurons release acetylcholine, a neurotransmitter that activates nicotinic acetylcholine receptors on postganglionic neurons.
  • The postganglionic neurons of sweat glands release acetylcholine for the activation of muscarinic receptors.
  • The parasympathetic nervous system uses acetylcholine (ACh) as its chief neurotransmitter, although peptides (such as cholecystokinin) may act on the PSNS as a neurotransmitter.

• Ionotropic and Metabotropic Receptors

  • The prototypic ligand-gated ion channel is the nicotinic acetylcholine receptor .
  • It consists of a pentamer of protein subunits with two binding sites for acetylcholine which, when bound, alter the receptor's configuration and cause an internal pore to open.
  • Examples of metabotropic receptors include glutamate receptors, muscarinic acetylcholine receptors, GABAB receptors, most serotonin receptors, and receptors for norepinephrine, epinephrine, histamine, dopamine, neuropeptides, and endocannabinoids.