BIOSCI107 · Biology for Biomedical Science: Cellular Processes and Development
Synaptic Transmission
Topic 6 continues into how neurons pass a signal on: the neuromuscular junction as the excitatory model, excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs), the neurotransmitter classes and how they are inactivated, and the spatial and temporal summation that lets tiny inputs add up to threshold. Examined in the 40% final exam (paper Teleform MCQ) — commonly as ordering the steps of transmission, distinguishing EPSP from IPSP, and reading a summation trace.
What this chapter covers
- 01The neuromuscular junction: presynaptic AP → voltage-gated Ca²⁺ influx → ACh release → ligand-gated cation channels → end-plate potential (always suprathreshold)
- 02Steps of chemical transmission: AP arrives → Ca²⁺ enters → vesicle exocytosis → transmitter binds receptor → postsynaptic potential
- 03EPSP (depolarising; glutamate/ACh; Na⁺/K⁺ channels) vs IPSP (hyperpolarising; GABA/glycine; K⁺ or Cl⁻)
- 04Neurotransmitter classes: small-molecule/classical (fast, direct — glutamate, GABA, glycine, ACh, amines) vs neuropeptides (slow, modulatory)
- 05Inactivation: diffusion, enzymatic degradation (acetylcholinesterase on ACh), and re-uptake by transporters
- 06Integration at the axon initial segment: each synapse gives a tiny (~0.1 mV) potential
- 07Temporal summation (rapid inputs from one synapse) and spatial summation (many synapses at once) to reach threshold
- 08Excitotoxicity: excess glutamate → Ca²⁺ overload → apoptosis (NMDA receptor)
Why a single synapse cannot fire a neuron — summation
- +1(a) Depolarisation needed = threshold − rest = (−55) − (−70) = 15 mV of net depolarisation to fire an action potential. [+1]
- +1(a) If each EPSP is about 0.1 mV, then roughly 15 ÷ 0.1 ≈ 150 simultaneous/overlapping EPSPs are needed — far more than one synapse delivers on its own. This is why a lone EPSP fails to trigger a spike; inputs must combine. [+1]
- +1(b) The two summation modes: temporal summation — one synapse fires rapidly so successive EPSPs overlap before each decays; and spatial summation — many synapses across the dendrites/soma fire together so their EPSPs add at the axon initial segment. Both push the membrane toward threshold; IPSPs subtract. [+1]
Key terms
- Neuromuscular junction (NMJ)
- The excitatory synapse between a motor neuron and a muscle fibre. A presynaptic action potential opens voltage-gated Ca²⁺ channels; Ca²⁺ triggers ACh release; ACh opens ligand-gated non-selective cation channels on the end plate, producing an end-plate potential that is always large enough to fire a muscle action potential.
- EPSP vs IPSP
- An excitatory postsynaptic potential is a small depolarisation (e.g. glutamate or ACh opening Na⁺/K⁺ channels) that moves the cell toward threshold; an inhibitory postsynaptic potential is a hyperpolarisation (e.g. GABA or glycine opening K⁺ or Cl⁻ channels) that moves it away. The neuron integrates both.
- Temporal summation
- Adding up postsynaptic potentials from a single synapse that fires rapidly, so each new EPSP arrives before the previous one has decayed. One of the two ways small inputs combine to reach threshold.
- Spatial summation
- Adding up postsynaptic potentials from many synapses firing at about the same time across the dendrites and soma, so their small depolarisations combine at the axon initial segment. The complement of temporal summation.
- Neurotransmitter inactivation
- The three ways a transmitter's signal is terminated: diffusion out of the cleft, enzymatic degradation (acetylcholinesterase breaks down ACh), and re-uptake by specific transporters (e.g. for glutamate, dopamine, serotonin). Without inactivation the signal would not reset.
- Excitotoxicity
- Damage caused by excessive excitatory signalling: too much glutamate over-activates NMDA receptors, flooding the neuron with Ca²⁺ and triggering apoptosis. Relevant to stroke and neurodegeneration (the drug riluzole limits it).
Synaptic Transmission FAQ
Why can one EPSP never fire an action potential?
Because a single EPSP (~0.1 mV) is tiny compared with the ~15 mV of depolarisation needed to go from rest (~−70 mV) to threshold (~−55 mV). A neuron therefore integrates many inputs: temporal summation adds rapid EPSPs from one synapse before they decay, and spatial summation adds EPSPs from many synapses firing together. Only when the combined depolarisation at the axon initial segment crosses threshold does a spike fire — and inhibitory IPSPs can subtract to prevent it. The neuromuscular junction is the exception: its single end-plate potential is always suprathreshold.
What is the difference between an EPSP and an IPSP?
An EPSP is excitatory — a small depolarisation that moves the membrane toward threshold, typically from glutamate or ACh opening channels permeable to Na⁺ (and K⁺). An IPSP is inhibitory — a hyperpolarisation (or stabilisation) that moves the membrane away from threshold, typically from GABA or glycine opening K⁺ or Cl⁻ channels. The postsynaptic neuron continuously sums EPSPs and IPSPs to decide whether to fire.
How is a neurotransmitter's signal switched off?
Three ways, and the exam likes to test them. The transmitter can simply diffuse out of the synaptic cleft; it can be enzymatically degraded (the classic example is acetylcholinesterase breaking down ACh at the NMJ); or it can be taken back up by specific re-uptake transporters (as for glutamate, dopamine and serotonin — the targets of many drugs). Without inactivation the receptors would stay activated and the synapse could not signal again.
Can AI help me with synaptic transmission in BIOSCI 107?
Yes, for study. Sia can order the steps of transmission, contrast EPSP and IPSP, drill the neurotransmitter classes and inactivation routes, and talk you through a summation trace. Use it to prepare for the final exam — it does not sit the exam for you, and the exam is an AI-free lane under the course's academic-integrity policy. Confirm the rules on Canvas.
Exam move
Learn transmission as an ordered sequence you can put in the right order under time pressure (AP arrives → voltage-gated Ca²⁺ enters → vesicle exocytosis → transmitter binds → postsynaptic potential), because 'sequence' items are common. Build a compact contrast set: EPSP vs IPSP (transmitter, ion, direction), small-molecule vs neuropeptide transmitters (fast/direct vs slow/modulatory), and the three inactivation routes (diffusion, enzyme, re-uptake) with acetylcholinesterase as the worked case. Understand integration conceptually — one ~0.1 mV EPSP cannot reach threshold, so the neuron uses temporal and spatial summation, with IPSPs subtracting — and practise reading summation traces. Keep the NMJ as the excitatory benchmark (its end-plate potential is always suprathreshold) and note excitotoxicity as the glutamate/Ca²⁺ pathology. This is exam material (Topic 6, Section C); confirm the exam date and Teleform format on Canvas.
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