Source: Understanding Neural Signaling: Membrane Potentials & Synaptic Transmission
Tags: synapse, chemical synapse, neurotransmission, synaptic transmission, neurotransmitter, glutamate, GABA, excitatory, inhibitory, EPSP, IPSP, synaptic cleft, vesicle, exocytosis, calcium, Ca2+, postsynaptic potential, summation, presynaptic terminal
When an action potential arrives at the end of an axon, it triggers a carefully sequenced chain of events that converts the electrical signal into a chemical one. Neurotransmitters cross the synaptic cleft and bind to receptors on the next neuron, producing either excitatory or inhibitory postsynaptic potentials. The receiving neuron sums all these inputs to decide whether to fire its own action potential.
Chemical synapse
A junction between two neurons where signalling occurs via neurotransmitter release. The presynaptic neuron sends the signal; the postsynaptic neuron receives it. A small gap (the synaptic cleft) separates the two.
Synaptic cleft
The narrow extracellular space (roughly 20–40 nm) between the presynaptic and postsynaptic membranes. Neurotransmitters diffuse across this gap to reach their receptors.
Presynaptic terminal (axon terminal / synaptic bouton)
The end of the sending neuron's axon, where synaptic vesicles filled with neurotransmitter are stored and released.
Synaptic vesicle
A small, membrane-bound sac in the presynaptic terminal that contains neurotransmitter molecules. Vesicles fuse with the presynaptic membrane during exocytosis to release their contents.
Exocytosis
The process by which vesicles merge with the presynaptic membrane and release neurotransmitter into the synaptic cleft. Triggered by a rise in intracellular Ca2+.
Voltage-gated calcium (Ca2+) channel
An ion channel in the presynaptic terminal that opens when the action potential arrives. The resulting influx of Ca2+ is the direct trigger for vesicle fusion and neurotransmitter release.
Neurotransmitter
A chemical messenger released by a presynaptic neuron that crosses the synaptic cleft and binds to receptors on the postsynaptic cell. Different neurotransmitters produce different effects.
Glutamate
The principal excitatory neurotransmitter in the central nervous system. Binding of glutamate to postsynaptic receptors causes depolarisation, making an action potential more likely.
GABA (gamma-aminobutyric acid)
The principal inhibitory neurotransmitter in the central nervous system. Binding of GABA to postsynaptic receptors causes hyperpolarisation, making an action potential less likely.
Excitatory postsynaptic potential (EPSP)
A small, graded depolarisation of the postsynaptic membrane caused by the opening of cation channels (typically allowing Na+ influx). Moves the membrane potential closer to threshold.
Inhibitory postsynaptic potential (IPSP)
A small, graded hyperpolarisation of the postsynaptic membrane, typically caused by the opening of Cl− channels or K+ channels. Moves the membrane potential further from threshold.
Summation
The process by which a neuron integrates multiple incoming postsynaptic potentials (both EPSPs and IPSPs) to determine whether the net depolarisation reaches threshold.
An action potential travels down the axon and arrives at the presynaptic terminal.
The depolarisation opens voltage-gated Ca2+ channels in the presynaptic membrane.
Ca2+ flows into the terminal, raising intracellular calcium concentration.
The rise in Ca2+ triggers synaptic vesicles to fuse with the presynaptic membrane (exocytosis), releasing neurotransmitter into the synaptic cleft.
Neurotransmitter molecules diffuse across the cleft and bind to specific receptors on the postsynaptic membrane.
Receptor binding opens ion channels in the postsynaptic membrane, producing either an EPSP or an IPSP depending on the type of receptor and the ions involved.
Excitatory transmission: Glutamate binds to receptors that allow Na+ (and sometimes Ca2+) into the postsynaptic cell, producing a depolarising EPSP. This brings the membrane closer to firing threshold.
Inhibitory transmission: GABA binds to receptors that allow Cl− into the cell (or K+ out), producing a hyperpolarising IPSP. This moves the membrane further from threshold, reducing the chance of an action potential.
Most neurons receive a mix of excitatory and inhibitory inputs simultaneously.
Temporal summation: Multiple signals from the same presynaptic neuron arrive in quick succession, and their EPSPs (or IPSPs) add together before decaying.
Spatial summation: Signals from different presynaptic neurons arrive at roughly the same time and combine at the postsynaptic cell.
The postsynaptic neuron acts as an integrator. If the net sum of all EPSPs and IPSPs at the axon hillock reaches threshold, the neuron fires an action potential. If not, it stays quiet.
Neurotransmitter action in the cleft must be stopped to prevent continuous stimulation. Common mechanisms include:
Reuptake: Transporter proteins on the presynaptic membrane pump neurotransmitter back into the terminal for recycling.
Enzymatic degradation: Enzymes in the cleft break down the neurotransmitter (e.g. acetylcholinesterase breaks down acetylcholine).
Diffusion: Neurotransmitter simply drifts away from the cleft.
⚠️ Ca2+ is the essential trigger for neurotransmitter release. Without Ca2+ influx into the presynaptic terminal, vesicles do not fuse and no signal crosses the synapse.
⚠️ Glutamate = main excitatory neurotransmitter; GABA = main inhibitory neurotransmitter. These are the two to know first. Expect questions that ask you to match each to its effect.
⚠️ EPSPs and IPSPs are graded potentials, not all-or-none. They vary in size and can sum together. This contrasts with action potentials, which are all-or-none.
⚠️ Summation (both temporal and spatial) is the mechanism by which the neuron "decides" whether to fire. Exam questions often present scenarios with varying numbers of excitatory and inhibitory inputs and ask whether threshold is reached.
⚠️ The postsynaptic response depends on the receptor, not just the neurotransmitter. The same neurotransmitter can be excitatory at one synapse and inhibitory at another if the receptor type differs.
Q: Describe the sequence of events at a chemical synapse, from the arrival of the action potential to the postsynaptic response.
A: The action potential depolarises the presynaptic terminal, opening voltage-gated Ca2+ channels. Ca2+ enters, triggering vesicle fusion with the membrane (exocytosis) and neurotransmitter release into the synaptic cleft. Neurotransmitter binds to postsynaptic receptors, opening ion channels that produce either an EPSP (depolarisation) or IPSP (hyperpolarisation).
Q: What is the role of calcium ions in synaptic transmission?
A: Ca2+ entering the presynaptic terminal through voltage-gated channels is the direct trigger for vesicle fusion and neurotransmitter release. Without Ca2+ influx, neurotransmitter is not released and the signal does not cross the synapse.
Q: How do EPSPs and IPSPs differ, and how does the neuron integrate them?
A: EPSPs are small depolarisations that move the membrane potential toward threshold (making firing more likely). IPSPs are small hyperpolarisations that move it away from threshold (making firing less likely). The neuron sums all incoming EPSPs and IPSPs through temporal and spatial summation. If the net depolarisation at the axon hillock reaches threshold, an action potential fires.
Q: A neuron receives 5 EPSPs and 3 IPSPs simultaneously. Under what condition would the neuron fire an action potential?
A: The neuron fires if the combined depolarisation from the 5 EPSPs, minus the combined hyperpolarisation from the 3 IPSPs, is sufficient to bring the membrane potential at the axon hillock to threshold (around −55 mV). The outcome depends on the relative magnitudes of each individual PSP.
Q: Name the two main neurotransmitters discussed and state whether each is excitatory or inhibitory.
A: Glutamate is the principal excitatory neurotransmitter (causes depolarisation). GABA is the principal inhibitory neurotransmitter (causes hyperpolarisation).
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