Structural Organization and Transmission Steps
Morphologically, the contact zone consists of three basic elements. The presynaptic membrane represents the boundary of the transmitting nerve terminal. The synaptic cleft is the microscopic space separating the cells. The postsynaptic membrane is the area of the innervated tissue directly adjacent to the nerve terminal.
The physiological process of signal transmission is divided into three sequential phases:
- Presynaptic stage. Inside the terminal, the chemical messenger is synthesized and stored in synaptic vesicles. An arriving nerve impulse causes membrane depolarization, which triggers exocytosis—the release of vesicle contents outward.
- Transit stage. Molecules of the chemical messenger diffuse through the aqueous medium of the synaptic cleft toward the receiving cell.
- Postsynaptic stage. The transmitter interacts with specific receptors on the membrane of the target organ. The result is a change in the effector cell's activity: inhibition or enhancement of its function.
Classification and Localization of Cholinergic Structures
Depending on the chemical nature of the released substance, cholinergic (transmitter is acetylcholine) and adrenergic (transmitter is norepinephrine) contacts are distinguished. Pharmacological agents acting on the efferent system are also divided into two main groups according to their target type.
Signal transmission via acetylcholine occurs in several key anatomical structures:
- In autonomic ganglia (transmission from preganglionic fibers).
- In internal organs (at the endings of postganglionic parasympathetic nerves).
- In skeletal muscle (neuromuscular junctions).
- In the adrenal medulla.
- In carotid bodies.
Life Cycle of Acetylcholine
The physiology of neurotransmitter turnover follows a strict sequence. Synthesis of molecules occurs in the cytoplasm of nerve terminals from acetyl-CoA and choline. The reaction is catalyzed by the enzyme choline acetyltransferase. The required choline is transported back into the neuron from the cleft via Na⁺-dependent transport. The synthesized substance is stored within vesicles.
The release process is triggered when the action potential reaches the axon terminal. Depolarization leads to the opening of voltage-gated calcium channels. An influx of $Ca^{2+}$ ions into the cytoplasm initiates the approximation and interaction of specific proteins: VAMPs (on vesicles) and SNAPs (on the cell membrane). Membrane fusion occurs, releasing acetylcholine into the cleft. This step can be pharmacologically blocked: for example, botulinum toxin destroys the fusion protein complex, whereas magnesium ions or aminoglycosides reduce calcium entry into the cell.
Once in the cleft, the neurotransmitter interacts with receptors on the postsynaptic side to conduct the impulse, as well as with receptors on the presynaptic membrane to control further substance release.
Enzymatic Inactivation of the Neurotransmitter
The action of acetylcholine is short-lived due to rapid neutralization systems. The primary pathway is hydrolysis. There are two types of enzymes with such activity:
- Acetylcholinesterase (true cholinesterase). Located directly within synapses, it provides rapid cleavage of the neurotransmitter into acetic acid and choline. The latter undergoes neuronal reuptake for reutilization.
- Butyrylcholinesterase (pseudocholinesterase, false cholinesterase). Located outside synaptic contacts—in blood plasma, liver, and other tissues. It is capable of destroying acetylcholine if it enters the systemic circulation.