Neural Control and Coordination · Lesson 5 of 8
Synapses: Passing Signals Between Neurons
“Electrical versus chemical synapses, vesicles, calcium, receptors, excitation, inhibition and transmitter clearance.”
• Define a synapse and distinguish its presynaptic and postsynaptic sides. • Compare direct electrical coupling with neurotransmitter-based transmission. • Trace the steps of chemical synaptic signalling from impulse arrival to postsynaptic response. • Explain why synaptic responses can be excitatory or inhibitory. • Describe how neurotransmitter signals end and why synapses are often directional.
An impulse reaches a terminal. What happens next?
An action potential conducts information along the membrane of one neuron. But the nervous system depends on thousands of connections between cells. A signal reaching the end of one axon must influence another neuron, a muscle fibre or a gland without simply becoming the same continuous axon. The specialised contact where this transfer occurs is a synapse.
A specialised functional junction through which one neuron communicates with another neuron or an effector cell.
The membrane of the signalling cell at the sending side of a synapse.
The receiving cell's membrane carrying receptors or other machinery responsive to the signal.
Synapses provide more than a physical crossing point. They allow one cell to excite or inhibit another, combine messages from many sources, alter the strength of communication through experience, and route information through networks. Not every axon contact produces an action potential in the next cell; that depends on the size, sign and combination of postsynaptic responses.
Two kinds of synaptic communication
At an electrical synapse, adjacent cells are linked by gap-junction channels formed from specialised membrane proteins. Ions and small currents can pass directly between cells, producing rapid coupling with little conventional synaptic delay. Some electrical connections transmit in both directions, while others can be directionally asymmetric. The source notes electrical synapses are relatively uncommon in the human nervous system compared with chemical synapses.
At a chemical synapse, the sending and receiving membranes are separated by a narrow extracellular synaptic cleft. An arriving action potential triggers release of neurotransmitter molecules from vesicles in the presynaptic terminal. The transmitter diffuses through the cleft and binds receptors on the receiving membrane. The receptor then changes ionic conductance or activates other cellular signalling routes. The chemical step introduces a small delay but permits extensive regulation and signal diversity.
The narrow extracellular gap between presynaptic and postsynaptic membranes at a chemical synapse.
A signalling chemical released from a presynaptic cell that binds receptors and alters the activity of a target cell.
A chemical synapse has a recognisable structure
The presynaptic axon terminal contains synaptic vesicles loaded with transmitter molecules, and its membrane contains release machinery and voltage-gated Ca²⁺ channels. The cleft separates it from the postsynaptic membrane, which contains specific receptors. Not all receptors are themselves ion channels; some activate second-messenger systems, while ligand-gated ion channels can act quickly. This difference explains how a chemical synapse can produce both fast and slower responses.
Figure 18.3 shows the synaptic knob, synaptic vesicles, presynaptic membrane, synaptic cleft, neurotransmitters, postsynaptic receptors and postsynaptic membrane. Every label reflects part of a process: vesicles carry the signal molecule, the cleft provides extracellular separation, and receptors give the target cell chemical specificity.
The steps of chemical synaptic transmission
First, an action potential reaches the presynaptic terminal and depolarises its membrane. Second, voltage-gated Ca²⁺ channels open, and Ca²⁺ enters because of the electrochemical gradient. Third, elevated terminal Ca²⁺ initiates docking and fusion of ready synaptic vesicles with the presynaptic plasma membrane. Fourth, transmitter molecules are released into the cleft by exocytosis. Fifth, they diffuse across the small gap and bind matching postsynaptic receptors.
Sixth, receptor activation changes the postsynaptic cell's electrical state or cellular signalling. In the simplest case the receptor opens ligand-gated ion channels and produces a graded postsynaptic potential. Seventh, transmitter action ends through diffusion away, enzymatic breakdown or uptake by the presynaptic terminal or nearby glial cells, depending on the transmitter. Vesicle membranes and transmitter supply are replenished so repeated signalling remains possible.
The source directly describes an action potential moving vesicles toward the terminal membrane, their fusion and release, receptor binding and changed postsynaptic ion flow. The role of Ca²⁺ is a physiological explanation of how arrival of the electrical impulse is coupled to vesicle fusion, strengthening the cause-and-effect account.
Excitatory versus inhibitory signalling
A graded postsynaptic change that makes the receiving neuron more likely to reach action-potential threshold under the prevailing conditions.
A graded postsynaptic change that reduces the receiving neuron's probability of reaching threshold, often by making the membrane more negative or stabilising its voltage.
Opening a postsynaptic channel does not automatically cause excitation. If receptor activation promotes inward positive current or another depolarising process, it may generate an EPSP. If it increases chloride or potassium conductance in ways that suppress depolarisation or promote hyperpolarisation, it may generate an IPSP. The effect depends on the receptor, ion gradients and cell type rather than the transmitter name alone.
A single small EPSP may not be enough to trigger a spike. Inputs from many synapses can summate in time and space, while inhibitory synapses can counterbalance excitation. This is how the next neuron integrates information and makes a controlled decision about generating an action potential.
Why chemical transmission is usually one-way
In a classical chemical synapse, vesicle release machinery is predominantly concentrated in the presynaptic terminal, whereas receptors for that transmitter are positioned mainly on the postsynaptic side. Thus signalling generally runs from releasing cell to receiving cell. This structural asymmetry explains why a typical chemical synapse is functionally directional. More complex circuits may use retrograde signals, but that does not erase the usual direction of the fast vesicle-mediated mechanism.
Electrical and chemical synapses compared
| Feature | Electrical synapse | Chemical synapse |
|---|---|---|
| Coupling | Direct ion flow through gap junctions | Chemical transmitter crosses cleft |
| Typical speed | Very little synaptic delay | Small delay from Ca²⁺, release and receptor steps |
| Direction | Often bidirectional; can be rectifying | Usually presynaptic → postsynaptic |
| Signal diversity | Direct electrical coupling | Excitation, inhibition and modulation |
| Key structure | Gap-junction channels | Vesicles, cleft and receptors |
How transmission ends
If neurotransmitter remained bound indefinitely, a synapse could not reliably communicate repeated changes. Synaptic enzymes may break down specific transmitters, transporters may reabsorb transmitters into neurons or glia, and diffusion can lower cleft concentration. The mechanism differs across synapses. For example, acetylcholinesterase rapidly breaks down acetylcholine at many neuromuscular junctions, while other transmitters are chiefly cleared by reuptake.
A nerve impulse is an electrical event within a neuron, not a chemical signal physically jumping from one axonal end to the next through empty space. At a typical chemical synapse, the signal changes form from electrical depolarisation to transmitter release and then to a new postsynaptic response. Electrical synapses provide a different shortcut through direct cell-cell coupling.
Problem
An action potential reaches a chemical synapse, but voltage-gated presynaptic Ca²⁺ channels cannot open. Explain the probable consequence.
- 1.The terminal may still conduct the arriving action potential.
- 2.Ca²⁺-dependent vesicle fusion and neurotransmitter release are greatly impaired.
- 3.Postsynaptic receptor activation and a resulting postsynaptic response are reduced or absent, depending on other pathways.
Quick Quiz
Quiz
What is the synaptic cleft?
Which ion typically enters a terminal to trigger vesicle fusion?
What is stored in presynaptic synaptic vesicles?
Which process transfers transmitter into the cleft?
What does an EPSP normally do?
Which feature characterises electrical synapses?
Why is a typical chemical synapse directional?
Which process can terminate transmitter action?
Practice Problems
- Trace chemical synaptic transmission step by step.
- Differentiate chemical and electrical synapses.
- Explain why a chemical synapse can inhibit rather than excite its target.
- Why does blocking presynaptic Ca²⁺ channels impair communication?
- Describe the main labelled elements in a chemical synapse diagram.
Action potential arrives → presynaptic depolarisation opens Ca²⁺ channels → Ca²⁺ triggers vesicle fusion → neurotransmitter enters cleft → binds postsynaptic receptor → ion conductance or signalling changes → transmitter is cleared.
Key Takeaways
• Synapses connect neurons with other neurons or effector cells. • Electrical synapses transfer current directly through gap-junction channels and are typically fast. • Chemical synapses have a presynaptic terminal, synaptic cleft and postsynaptic receptors. • An arriving impulse opens Ca²⁺ channels, leading to vesicle fusion and neurotransmitter release. • Transmitter binding can produce excitatory or inhibitory postsynaptic changes. • Typical chemical transmission is directional because releasing and receiving machinery are asymmetrically distributed. • Reuptake, enzymatic breakdown and diffusion help end synaptic signals.