At a synapse, nerve signals switch from electrical to chemical: the presynaptic neurone releases neurotransmitter molecules into the synaptic cleft, they diffuse across and bind to receptors on the postsynaptic membrane, triggering a new electrical impulse. This chemical relay gives the nervous system precise control over signal transmission.
What is a synapse?
A synapse is a junction between two neurones, or between a neurone and an effector (such as a muscle or gland). Neurones do not physically touch — there is a tiny gap of about 20 nanometres called the synaptic cleft separating them.
The neurone arriving at the synapse is the presynaptic neurone; the one leaving is the postsynaptic neurone. The presynaptic terminal contains many small membrane-bound packages called synaptic vesicles, each packed with chemical neurotransmitter molecules. The postsynaptic membrane carries receptor proteins shaped to match the neurotransmitter.
How do neurotransmitters transmit a signal across the synapse?
The sequence of events at a synapse is as follows:
- An electrical impulse (action potential) travels along the presynaptic neurone and arrives at the synaptic knob.
- The impulse causes calcium ions to enter the synaptic knob through ion channels in the membrane.
- The calcium ions cause synaptic vesicles to fuse with the presynaptic membrane, releasing neurotransmitter into the synaptic cleft by exocytosis.
- The neurotransmitter molecules diffuse across the cleft (a very short distance — this takes only a fraction of a millisecond).
- The neurotransmitter binds to complementary receptor proteins on the postsynaptic membrane.
- Binding opens ion channels in the postsynaptic membrane, allowing ions to flow in or out and generating a new electrical impulse.
What happens to the neurotransmitter after it binds?
The neurotransmitter cannot remain bound indefinitely — a continuous signal would be uncontrolled. The neurotransmitter is removed by one of two mechanisms:
- Enzymatic breakdown: specific enzymes in the synaptic cleft break the neurotransmitter down into inactive fragments. For example, the enzyme acetylcholinesterase breaks down acetylcholine into choline and acetic acid.
- Reuptake: the neurotransmitter is reabsorbed back into the presynaptic neurone through transporter proteins and recycled into new vesicles.
Both mechanisms terminate the signal so that the nervous system can respond to the next stimulus.
What are the key neurotransmitters in GCSE biology?
| Neurotransmitter | Where it acts | Main role |
|---|---|---|
| Acetylcholine (ACh) | Neuromuscular junctions; CNS; parasympathetic NS | Stimulates muscle contraction; slows heart rate |
| Adrenaline | Released by adrenal glands into blood (hormone); also at synapses | "Fight or flight" — raises heart rate, dilates pupils |
| Dopamine | Brain reward pathways | Mood, reward, motivation |
| Serotonin | Brain | Mood regulation, sleep, appetite |
At GCSE you are expected to know acetylcholine in detail and be aware that different neurotransmitters have different effects.
How do synapses allow the nervous system to control signals?
Synapses are not simply junctions — they are decision points:
- Summation: a single presynaptic neurone may not release enough neurotransmitter to trigger a postsynaptic impulse. Several neurones firing simultaneously can release enough between them to surpass the threshold — this is spatial summation.
- Signal direction: neurotransmitter vesicles are only on the presynaptic side, so signals can only travel in one direction across a synapse. This prevents nerve impulses travelling backwards.
- Divergence and convergence: one presynaptic neurone can connect to many postsynaptic neurones (divergence), allowing one signal to trigger many responses; many neurones can converge on a single postsynaptic neurone, integrating information.
How do drugs affect synaptic transmission?
Many drugs work by mimicking, enhancing, or blocking neurotransmitters at synapses:
| Drug | Mechanism | Effect |
|---|---|---|
| Nicotine | Binds ACh receptors in brain | Mimics acetylcholine — stimulant effect; addictive |
| Caffeine | Blocks adenosine receptors | Prevents drowsiness; increases alertness |
| Ecstasy (MDMA) | Blocks serotonin reuptake transporters | More serotonin remains in cleft; elevated mood |
| Beta blockers | Block adrenaline (noradrenaline) receptors in the heart | Reduce heart rate; used in anxiety and hypertension |
| Prozac (fluoxetine) | Blocks serotonin reuptake (SSRI) | Increases serotonin in cleft; used in depression |
Understanding synaptic mechanisms explains both therapeutic drug design and why recreational drugs can be addictive.
Frequently asked questions
What is the difference between a neurotransmitter and a hormone?
Both are chemical messengers, but they differ in how they travel. A neurotransmitter is released directly into the synaptic cleft — a gap of only ~20 nm — and acts on receptors on the adjacent postsynaptic membrane within milliseconds. A hormone is secreted by an endocrine gland into the bloodstream and travels throughout the body, taking seconds to minutes to reach its target cells. Adrenaline is unusual: it acts as a neurotransmitter at some synapses and as a hormone when released by the adrenal glands into the blood.
Why can nerve signals only travel in one direction across a synapse?
Synaptic vesicles containing neurotransmitter are found only on the presynaptic side of the synapse, never on the postsynaptic side. Receptor proteins that respond to the neurotransmitter are only on the postsynaptic membrane. Because the chemical signal can only flow from presynaptic to postsynaptic, the electrical signal triggered by binding can only travel in one direction — away from the previous neurone.
Why is acetylcholinesterase important at neuromuscular junctions?
After acetylcholine binds to receptors on the muscle fibre membrane and triggers a contraction, the muscle must be able to relax. Acetylcholinesterase, located in the synaptic cleft, rapidly breaks down acetylcholine into choline and acetic acid. This terminates the stimulus and allows the muscle to stop contracting. Without this enzyme, the muscle would remain in constant contraction (tetanic). Many nerve-agent poisons (such as sarin) work by inhibiting acetylcholinesterase, which is why they are so dangerous.
How does ecstasy (MDMA) affect the brain?
MDMA blocks the reuptake transporters for serotonin on the presynaptic membrane, so serotonin accumulates in the synaptic cleft and continues to bind postsynaptic receptors. This leads to prolonged activation of serotonin pathways associated with mood, empathy, and pleasure. Over time, the brain may down-regulate (reduce the number of) serotonin receptors in response to the excess stimulation, which can cause depression when the drug wears off and is one reason repeated use can harm mental health.
For Socratic GCSE biology with Professor Darwin — tracing nerve signals from synapse to system to behaviour — visit aitutors.me.