Synaptic transmission

Overview

A synapse is a junction where one neuron passes a signal to another neuron (or to a muscle or gland).

There are two kinds:

• Chemical synapses: use a neurotransmitter. Almost all synapses in the human nervous system are chemical.
• Electrical synapses: current flows directly through gap junctions.

The chemical synapse

Structure

• Presynaptic terminal: contains vesicles of transmitter and many mitochondria.
• Synaptic cleft: a gap of about 20–30 nm.
• Postsynaptic membrane: has receptor proteins.

Steps of transmission

1. An action potential reaches the presynaptic terminal.
2. Voltage-gated Ca2+ channels open; Ca2+ enters.
3. Ca2+ causes vesicles to fuse with the membrane and release transmitter by exocytosis.
4. The transmitter diffuses across the cleft and binds to receptors.
5. Ion channels open (or second messengers are activated), changing the postsynaptic potential.
6. The transmitter is removed: broken down by enzymes, taken back up into the terminal, or diffuses away.

Postsynaptic potentials

Excitatory postsynaptic potential (EPSP)

The transmitter opens channels that let Na+ in, making the membrane less negative. The cell moves closer to threshold.

A single EPSP is small (about 0.5–1 mV). Many are needed to fire the neuron.

Inhibitory postsynaptic potential (IPSP)

The transmitter opens Cl− channels (Cl− in) or K+ channels (K+ out), making the membrane more negative (hyperpolarised). The cell moves further from threshold.

Where the action potential starts

Postsynaptic potentials spread passively over the cell body. The action potential starts at the axon initial segment (axon hillock), which has many voltage-gated Na+ channels and the lowest threshold.

Summation

A neuron adds up all its inputs.

• Spatial summation: EPSPs from many different synapses at the same time add together.
• Temporal summation: repeated firing of the same synapse quickly, so each new EPSP adds to the last before it fades.

If the sum reaches threshold at the initial segment, the neuron fires. IPSPs subtract from the total.

Types of inhibition

• Postsynaptic inhibition: an IPSP on the postsynaptic cell.
• Presynaptic inhibition: an inhibitory neuron synapses on the presynaptic terminal of another neuron and reduces its transmitter release (often by GABA opening Cl− channels on the terminal). It controls one input without affecting others. It is important in pain control and sensory pathways.

Special properties of synapses

• One-way conduction: transmitter is released only from the presynaptic side, so signals pass in one direction.
• Synaptic delay: about 0.5 ms per synapse for release, diffusion and receptor binding. The number of synapses in a pathway can be estimated from the delay.
• Synaptic fatigue: with very rapid, repeated firing, the transmitter store is used up and transmission weakens. This helps stop epileptic seizures.
• Post-tetanic facilitation: after a burst of rapid stimulation, the synapse responds more strongly for a while (extra Ca2+ in the terminal).
• Effect of pH: alkalosis increases neuronal excitability (can trigger seizures); acidosis decreases it (coma in severe acidosis).
• Hypoxia quickly stops synaptic transmission; consciousness is lost within seconds when brain blood flow stops.

Electrical synapses

Cells are joined by gap junctions made of connexin proteins. Ions flow directly from one cell to the next.

• Very fast, with no delay.
• Can conduct in both directions.
• Synchronise groups of cells.
• Found in cardiac muscle, smooth muscle and some parts of the brain.

Main neurotransmitters

Small-molecule transmitters act quickly; neuropeptides are made in the cell body, act slowly and have long-lasting effects. A neuron may release both.

Clinical relevance

Tetanus

How it happens: tetanus toxin blocks the release of the inhibitory transmitters glycine and GABA in the spinal cord.

What you see: severe muscle spasms and rigidity (lockjaw).

Strychnine poisoning

How it happens: strychnine blocks glycine receptors.

What you see: violent convulsions, similar to tetanus.

Benzodiazepines

How it happens: they enhance the action of GABA at GABA-A receptors (more Cl− entry).

What you see: calming, sedation and anticonvulsant effects.

Epilepsy

How it happens: too much excitation or too little inhibition in cortical networks.

What you see: seizures; many antiepileptic drugs boost GABA or reduce glutamate action or Na+ channel activity.

Quick revision

• Ca2+ entry triggers transmitter release.
• EPSP: Na+ in. IPSP: Cl− in or K+ out.
• Spatial: many synapses at once. Temporal: one synapse repeatedly.
• Action potential starts at the axon initial segment.
• Synaptic delay about 0.5 ms; chemical synapses are one-way.
• Glutamate excites; GABA (brain) and glycine (cord) inhibit.
• Gap junctions: electrical synapses, fast, two-way.

Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).

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