Question

can you please repeat the acetylcholine?

- I should talk about its synthesis- (physiologic mechanisms and drugs or foods affecting them);

- storage in vesicles (physiology-like the name of the pump for storage and drugs, toxins or foods that interferes with it);

-its release-physiology and drugs or toxins that interfere;

-the termination of effect in the synapse (physiology-like enzymatic breakage or re-uptake

-about the drugs that affect the process  

-and its receptors of these neurotransmitters and drugs acting on these receptors -refer them as agonists and antagonists for relevant receptors).

i don't need it with figures, only a clear explanation, please!

Answer 1

Acetylcholine

An important neurotransmitter called acetylchloline is inevitable in autonomic nervous system. It acts as the final released NT of parasympathetic nervous system and as an internal transmitter for the sympathetic nervous system.

It is synthesized by enzymatic action of choline acetyltransferase from the precursors called choline and acetyl-CoA. Neurons which are capable of producing ACh are called as cholinergic neurons and the major cholinergic area is the nucleus basalis of Meynert in the basal forebrain. Cholinergenic neuronal action is inhibited by binding to oligomers of the amyloid-β peptide (Aβ) which in turn inhibit choline acetyltransferase (ChAT) that might impair acetylcholine production.

The secreted ACh are stored in vesicles called cholinergic vesicles which are stored at the nerve ending until an action potential arrives and allows for its release into the synaptic cleft.

ACh is released when AP arrives at the presynaptic terminal which triggers the release of ACh from its vesicle. Once released there are diffused to the post synaptic cell where they bind to receptors to exerts its effect. Two major types of receptors are nicotinic and muscarinic. Nicotinic receptors are ligand-gated ion channels permeable to sodium, potassium, and calcium ions whereas muscarinic acetylcholine receptors has longer effects and more complex mechanism.

The excess ACh has to be cleared from the synaptic cleft to keep the contraction progressed otherwise end up in signal jam. It is done by the enzyme acetylcholinesterase that converts acetylcholine into the inactive metabolites called choline and acetate. Neurotoxin that selectively inhibit  acetylcholinesterase causes excess accumulation of acetylcholine at the neuromuscular junction.

ACh is the priamary NT for skeletal muscle contraction and released from at ynaptic cleft of NMJ. These are the muscles used for all types of voluntary movement. They are controlled by motor neurons located in the spinal cord or sometimes, brain stem.

ACH agonist: nicotinic agonist - mimics the action of ACh at nicotinic acetylcholine receptors (nAChRs). Examples are epibatidine, lobeline, varenicline and cytisine.

ACh antagonist: Muscarinic antagonist receptors - lowers the parasympathetic activity - Atropine.