25 topics with concise breakdowns: definitions, key facts, and class questions.
This section focuses on drugs that affect nerve impulse transmission via acetylcholine. First, we will review the basic theory: the structure and physiology of synapses, as well as the localization and effects of stimulating M- and H-cholinergic receptors.
The articles provide a detailed breakdown of all key groups of cholinotropic drugs. You will study direct and indirect cholinomimetics (including pilocarpine and anticholinesterase agents), M-anticholinergics (from the reference drug atropine to selective agents like pirenzepine and tiotropium bromide), ganglionic blockers, and muscle relaxants of various mechanisms of action. Special attention is paid to the use of drugs in ophthalmology, botulinum toxin, and the clinically significant interactions of cholinotropic agents.
Please note: during classes and exams, professors most frequently expect a precise knowledge of atropine pharmacodynamics, the mechanism of action of neostigmine, the differences between depolarizing and nondepolarizing muscle relaxants, as well as the clinical presentation and antidote therapy for organophosphate (OP) poisoning.
This is the process by which synaptic vesicles fuse with the presynaptic membrane and release their contents into the synaptic cleft. It is triggered when calcium ions enter the cytoplasm of the nerve terminal following membrane depolarization.
Why are vascular M3-cholinergic receptors called non-innervated?
Because they are located on the vascular endothelium outside synaptic clefts and do not receive direct nerve impulses. They are activated exclusively by agonist substances present in the bloodstream.
How does an ionotropic receptor differ from others?
An ionotropic receptor is directly coupled to an ion channel (in this case, a sodium channel). Upon binding with the neurotransmitter, it directly opens the pore for ions, ensuring a very high speed of signal transmission without the involvement of complex intracellular cascades.
Why is pilocarpine rarely prescribed orally?
It is a non-polar tertiary amine, easily crosses the blood-brain barrier, and causes severe CNS excitation up to convulsions. It is administered orally only in small doses for severe xerostomia (dry mouth).
What is the main difference between tertiary and quaternary M-cholinomimetics?
Tertiary amines (e.g., aceclidine) do not carry a permanent ionic charge. This allows them to penetrate biological membranes much better compared to quaternary compounds.
Why does nicotine cause strong dependence?
It is highly lipophilic, easily crosses the blood-brain barrier, and stimulates dopamine release in the CNS, causing pleasurable sensations. When administration ceases, a severe withdrawal syndrome and psychological dependence develop.
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