Preparation for transmission: synthesis and storage
For uninterrupted synaptic function, the neurotransmitter must be prepared in advance. One part of the required pool is synthesized directly in the nerve cell body and then delivered to the presynaptic terminal via axonal transport (at a rate of about 40 cm per day). Another part is produced directly on-site, within the presynaptic terminal itself.
To prevent neurotransmitter molecules from diffusing into the cytoplasm and to ensure they are ready for instant release, they are enclosed by membranes and packaged into tiny vesicles—synaptic vesicles. In this form, they are stored in the presynaptic terminal, awaiting the arrival of a nerve impulse.
Main stages of signal transmission
The process of information transfer in chemical synapses is strictly ordered and requires the participation of calcium ions. It includes the following steps:
- Arrival of the impulse. An action potential (AP) travels along the axon to the presynaptic terminal. Membrane depolarization occurs due to the influx of $Na^+$ ions.
- Calcium influx. The charge change opens voltage-gated calcium channels, and $Ca^{2+}$ ions rush into the terminal.
- Exocytosis. Calcium ions act as a key factor: under their influence, vesicles move to the active zones of the presynaptic membrane, fuse with it, and release portions of the neurotransmitter directly into the synaptic cleft.
- Diffusion and binding. Through passive diffusion, neurotransmitter molecules cross the cleft and bind to specific protein-lipid receptors on the postsynaptic membrane.
Response formation: excitation and inhibition
The interaction of the neurotransmitter with receptors determines whether the signal will proceed further or be blocked.
In excitatory synapses, the neurotransmitter opens pores for $Na^+$ ions. Sodium enters the cell, causing depolarization. This produces an excitatory postsynaptic potential (EPSP) (amplitude 1–50 mV, duration 10–100 ms). Local currents from the summed EPSP generate a full-scale AP in adjacent membrane regions, and excitation is conducted further.
In inhibitory synapses (where GABA, glycine, and in the autonomic system also acetylcholine and noradrenaline operate), membrane permeability increases for $K^+$ and $Cl^-$ ions. Potassium leaves the cell, and chloride enters along its concentration gradient. This leads to hyperpolarization and the development of an inhibitory postsynaptic potential (IPSP). The threshold of excitation increases, excitability drops, and signal conduction is blocked.
Fate of the neurotransmitter and properties of synapses
For the synapse to receive the next signal, the synaptic cleft must be cleared of the spent neurotransmitter. This occurs via three pathways:
- Enzymatic degradation. Specific enzymes break down the neurotransmitter (for example, acetylcholine is degraded by cholinesterase, and noradrenaline is broken down sequentially by COMT and MAO).
- Reuptake. Most of the breakdown products are actively reabsorbed back into the presynaptic terminal for resynthesis.
- Diffusion and control. Part of the substance is lost, while another part binds to presynaptic autoreceptors, which assess the release volume and regulate it via negative feedback.
It is these mechanisms that determine the key functional properties of synapses: unidirectional conduction (from the pre- to the postsynaptic membrane), high chemical sensitivity to biologically active substances, and synaptic delay, which is spent on the release and diffusion of molecules.
Briefly: answers to topical questions
Which specific proteins ensure the fusion of the synaptic vesicle with the presynaptic membrane?
The fusion of the synaptic vesicle with the presynaptic membrane is mediated by proteins of the SNARE complex:
- SNAP-25 and syntaxin are proteins of the presynaptic membrane;
- synaptobrevin is a protein of the vesicle membrane.
What is the average duration of a synaptic delay in milliseconds?
The average duration of a synaptic delay in a chemical synapse ranges from 0.2 to 0.5 ms. In an electrical synapse, the response on the postsynaptic membrane occurs faster, with a delay of approximately 0.1 ms. This time is predominantly spent on the diffusion of the neurotransmitter across the synaptic cleft from the presynaptic to the postsynaptic membrane.
How do ionotropic receptors of the postsynaptic membrane differ from metabotropic ones?
The main difference between the receptors lies in the mechanism of their effector action and the speed at which the response develops.
| Characteristic | Ionotropic mechanism | Metabotropic mechanism |
|---|---|---|
| Speed of action | Fast-acting | Slow-acting |
| Principle of operation | Effector proteins function as ion channels | Alters intracellular processes within the postsynaptic cell via secondary messengers |
| Examples of receptors | Nicotinic acetylcholine receptors, $GABA_A$ | Muscarinic acetylcholine receptors, adrenoceptors |
For quick memorization of ion mechanisms: Sodium Starts (depolarization, EPSP), while Potassium and Chloride Calm (hyperpolarization, IPSP).
Class and exam questions
Why is excitation in a synapse transmitted in only one direction?
Unidirectional conduction is due to structural features: the neurotransmitter is released only from the presynaptic terminal, and receptors capable of responding to it are located exclusively on the postsynaptic membrane.
What is the main physiological role of calcium ions in the synapse?
$Ca^{2+}$ ions are a key trigger for exocytosis. Entering the presynaptic terminal upon depolarization, they cause vesicles to move toward the membrane and release the neurotransmitter into the synaptic cleft.
How does IPSP differ from EPSP?
EPSP (excitatory potential) is associated with sodium influx and depolarization, leading to the generation of a nerve impulse. IPSP (inhibitory potential) is caused by potassium and chloride currents, which induce hyperpolarization and block signal conduction.
What else to study on this topic
- Mechanisms of neurotransmitter reuptake
- Enzymatic inactivation of noradrenaline: the role of COMT and MAO
- Spatial and temporal summation of EPSP
- Presynaptic autoreceptors and negative feedback
- Neurotransmitters of inhibitory synapses in the autonomic nervous system
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