Properties of Synapse

Simple diagram (chemical synapse)

   PRESYNAPTIC NEURON (axon terminal)
   ┌─────────────────────────────┐
   │  Action potential arrives   │
   │            ↓                │
   │   Ca2+ channels open        │
   │            ↓                │
   │  ( o ) ( o ) ( o )          │  ← synaptic vesicles
   │   (with neurotransmitter)   │     (contain neurotransmitter)
   └──────────────┬──────────────┘
          exocytosis ↓ ↓ ↓          
   ═══════════ SYNAPTIC CLEFT ═══════════  (20-30 nm)
            transmitter diffuses ↓
   ──────────────[ ] [ ] [ ]─────────────  ← receptors
   POSTSYNAPTIC MEMBRANE (dendrite / soma)
            ↓
   EPSP (Na+ in) or IPSP (Cl- in / K+ out)

Properties of synapse

1. One-way conduction (valve action)
   • The impulse passes only from presynaptic to postsynaptic neuron.
   • Vesicles and transmitter are present only in the presynaptic terminal, and receptors are only on the postsynaptic membrane.
   • This is the Bell-Magendie law.
2. Synaptic delay
   • Transmission across a synapse takes at least 0.5 ms.
   • The delay is the time needed to release the transmitter, diffuse across the cleft and act on the receptors.
   • More synapses in a pathway make conduction slower. Measuring the delay shows whether a reflex is monosynaptic or polysynaptic (Ganong's Review of Medical Physiology, 26th ed.).
3. Summation
   • Spatial: several presynaptic inputs arrive together, so the EPSPs add up.
   • Temporal: inputs arrive in rapid succession and overlap in time.
   • If an excitatory and an inhibitory input arrive together, they cancel each other (Costanzo Physiology, 7th ed.).
4. Fatigue
   • With repeated stimulation, the postsynaptic response becomes smaller than expected.
   • The likely cause is depletion of transmitter stores in the presynaptic terminal (Costanzo Physiology, 7th ed.).
   • Synapses fatigue before nerve fibres do. This is why prolonged seizures stop.
5. Facilitation, post-tetanic potentiation and long-term potentiation (LTP)
   • Repeated stimulation gives a greater response than expected.
   • The mechanism is increased transmitter release, possibly because Ca2+ accumulates in the terminal.
   • LTP is involved in memory storage (Costanzo Physiology, 7th ed.).
6. Convergence and divergence
   • Convergence: many presynaptic neurons end on one postsynaptic neuron.
   • Divergence: one neuron branches to supply many neurons, which amplifies the signal.
7. Inhibition
   • Postsynaptic inhibition produces an IPSP, for example through GABA or glycine.
   • Presynaptic inhibition reduces transmitter release.
8. Susceptibility to drugs, pH and hypoxia
   • Synapses are the most easily affected part of the nervous system.
   • Hypoxia and acidosis depress transmission.
   • Alkalosis increases excitability and can cause seizures.
   • Strychnine blocks glycine receptors.
   • Tetanus toxin blocks release of GABA and glycine.
   • Botulinum toxin blocks acetylcholine release.
   • Caffeine increases excitability.
   • Anaesthetics decrease excitability.
9. Plasticity
   • Synapses change with use. The change can be short-term or long-term, and it underlies learning.

Quick memory aid: "O-D-S-F-C-I-S"

1. Presynaptic terminal: it contains mitochondria and synaptic vesicles filled with neurotransmitter.
2. Voltage-gated Ca2+ channels: Ca2+ enters when the action potential arrives. This triggers vesicle fusion and exocytosis.
3. Synaptic cleft: the gap of about 20-30 nm that the transmitter diffuses across.
4. Postsynaptic membrane with receptors: the transmitter binds here and produces an EPSP or IPSP.
5. Arrow showing one-way direction: from presynaptic to postsynaptic only.