ACh

Acetylcholine (ACh) is a chemical neurotransmitter used by the central nervous system (CNS) as well as the peripheral nervous system (PNS). Acetylcholine is a classical neurotransmitter and, in fact, it was the first of the classic neurotransmitters to be discovered. It was discovered in 1914 by Henry Hallett Dale while conducting experiments on the heart.

Acetylcholine is the neurotransmitter used by the somatic division of the nervous system at the neuromuscular junction (where a somatic motor neuron makes synaptic contact with a skeletal muscle cell). Acetylcholine is also used extensively by both branches of the autonomic nervous system; sympathetic and parasympathetic. It is the primary neurotransmitter released in autonomic ganglia by preganglionic autonomic neurons. It is also the primary neurotransmitter released by parasympathetic postganglionic neurons. A few sympathetic postganglionic neurons also release acetylcholine. The diverse actions of acetylcholine are exerted via the activation of nicotinic and muscarinic ACh receptors.

Acetylcholine (Wikipedia)

An enzyme found in the synaptic cleft at cholinergic synapses. It degrades acetylcholine to choline and acetate and, thus, terminates the action of acetylcholine at the synapse. Neither choline nor acetate can bind to acetylcholine receptors (nicotinic or muscarinic).

An agonist is a molecule that binds to a receptor and activates a physiological response similar to that induced by the naturally occurring physiological ligand of the receptor. Therefore, agonist binding to a receptor mimics the action of the natural ligand.

For example, acetylcholine (ACh) is the naturally occurring physiological ligand that activates nicotinic and muscarinic acetylcholine receptors. Nicotine is an agonist of nicotinic ACh receptors (nAChR), and muscarine is an agonist of muscarinic ACh receptors (mAChR).

Antagonist

An antagonist is a molecule that binds to a receptor, however, it does not activate the physiological response induced by the naturally occurring physiological ligand of the receptor. Moreover, once bound to the receptor, an antagonist prevents the physiological ligand from activating the receptor. Therefore, antagonist binding to a receptor prevents or blocks the action of the natural ligand.

For example, acetylcholine (ACh) is the naturally occurring physiological ligand that activates nicotinic and muscarinic acetylcholine receptors. Tubocurarine and succinylcholine are antagonists of the nicotinic ACh receptor (nAChR), and atropine is an antagonist of the muscarinic ACh receptor (mAChR).

Agonist

Refers to neurons, synapses, or receptors where acetylcholine is used as the neurotransmitter.

For example, cholinergic neurons release acetylcholine as their neurotransmitter.

In cholinergic synapses, acetylcholine is released from the presynaptic neuron, and it acts on acetylcholine receptors in the plasma membrane of the postsynaptic cell.

Cholinergic receptors are those that respond to acetylcholine as the physiological ligand. The two major types are nicotinic and muscarinic cholinergic receptors (may also be referred to as nicotinic and muscarinic acetylcholine receptors).

Cholinergic drugs are compounds that mimic the action of acetylcholine by binding to and activating cholinergic receptors.

A potent blocker of nicotinic cholinergic receptors (nicotinic acetylcholine receptor, nAChR) found at the neuromuscular junction. At small doses, curare can lead to muscle weakness. At high doses, curare can lead to paralysis of skeletal muscles, which would also result in asphyxiation (and ultimately death) due to paralysis of the diaphragm. Curare was commonly the active agent of poison arrow.

See Wikipedia

Neurotoxins are chemical molecules that have an adverse effect on neuron function and, thus, disrupt the normal function of the nervous system. Neurotoxins could be small molecules or peptides and can be derived from a variety of invertebrate and vertebrate animals, as well as plant species.

The following is a short list of some examples of neurotoxins:

α-Bungarotoxin: A peptide neurotoxin that inhibits the nicotinic acetylcholine receptor.

Chlorotoxin: A peptide neurotoxin that inhibits chloride channels.

α-Conotoxin: A peptide neurotoxin that inhibits the nicotinic acetylcholine receptor.

δ-Conotoxin: A peptide neurotoxin that inhibits voltage-gated sodium channels.

w-Conotoxin: A peptide neurotoxin that inhibits N-type voltage-gated calcium channels.

Picrotoxin: Inhibits GABA_A receptor chloride channels.

Tetrodotoxin: Inhibitor of neuronal voltage-gated sodium channels.