Generation of an Excitatory Postsynaptic Potential
- Recall that a synapse is a junction between two neurons or between a neuron and an effector cell (like a muscle or gland).
- When a nerve impulse reaches the end of a neuron, it can’t simply jump to the next cell.
- Instead, it relies on neurotransmitters, chemical messengers that carry the signal across the synaptic gap.
The synaptic gap is incredibly narrow, only about 20–40 nm wide, which is just two to four times the thickness of a typical cell membrane.
Steps in the Generation of an EPSP Using Acetylcholine
Release of Acetylcholine
- When an action potential reaches the presynaptic terminal of a motor neuron, acetylcholine is released into the synaptic cleft through exocytosis.
- Acetylcholine travels across the synaptic cleft and binds to acetylcholine receptors located on the postsynaptic membrane of the muscle cell or next neuron.
Binding to Transmembrane Receptors
- Acetylcholine binds to specific ligand-gated ion channels (also called nicotinic receptors) on the postsynaptic membrane.
- This binding causes the ion channels to open, allowing sodium (Na⁺) ions to flow into the postsynaptic cell.
- In the case of acetylcholine, binding to its receptor opens sodium ($\text{Na}^+$) channels.
- Sodium ions then flow into the postsynaptic cell, making the inside of the cell less negative.
Depolarization of the Postsynaptic Membrane
- The influx of positively charged sodium ions (Na⁺) makes the inside of the postsynaptic cell more positive.
- This results in depolarization of the postsynaptic membrane, which is the characteristic feature of an EPSP.
Generation of EPSP
- The EPSP is a small, localized depolarization that may be enough to bring the membrane potential closer to the threshold for an action potential.
- If the depolarization reaches the threshold at the axon hillock of the postsynaptic neuron, it will trigger the generation of an action potential.
Termination of the Signal
- The acetylcholine signal is terminated by the enzyme acetylcholinesterase, which breaks down acetylcholine in the synaptic cleft, preventing continuous stimulation of the postsynaptic membrane.
- The breakdown products are taken back into the presynaptic neuron for recycling.
- Diffusion is a passive process, meaning it doesn’t require energy.
- This allows neurotransmitters to cross the synaptic cleft rapidly.
Neurotransmitter Receptors Open Ion Channels to Alter Membrane Potential
- Many neurotransmitter receptors are linked to ion channels.
- When a neurotransmitter binds to its receptor, it causes the ion channel to open, allowing ions to flow into the postsynaptic cell.
EPSPs Reduce Membrane Potential to Trigger Action Potentials
- The influx of positive ions (like sodium) reduces the negative charge inside the postsynaptic neuron.
- This change in charge is called an excitatory postsynaptic potential (EPSP).
- If the EPSP is strong enough, it can trigger an action potential in the postsynaptic neuron, allowing the signal to continue.
Excitatory Postsynaptic Potential (EPSP)
A depolarizing change in the postsynaptic membrane potential that makes the postsynaptic cell more likely to fire an action potential.
Not all neurotransmitters are excitatory. Some cause the postsynaptic membrane to become more negative, making it less likely to fire an action potential. These are called inhibitory neurotransmitters.
Acetylcholine Triggers Muscle Contraction by Creating an EPSP
Acetylcholine
Acetylcholine is a neurotransmitter found in many types of synapses, including neuromuscular junctions (where nerves connect to muscles).
- When acetylcholine binds to its receptor on the postsynaptic membrane, it opens sodium channels.
- Sodium ions flow into the cell, creating an EPSP.
- If the EPSP reaches a certain threshold, it triggers an action potential in the muscle cell, causing it to contract.
- Don’t confuse the terms presynapticand postsynaptic.
- The presynaptic neuron releases the neurotransmitter, while the postsynaptic neuron (or effector cell) receives the signal.
Acetylcholinesterase Stops Stimulation by Breaking Down Acetylcholine
- To prevent continuous stimulation, acetylcholine is quickly broken down by an enzyme called acetylcholinesterase.
- This enzyme splits acetylcholine into choline and acetate.
- The choline is reabsorbed by the presynaptic neuron and used to synthesize more acetylcholine.
- Imagine pouring water into a glass.
- The reason water forms droplets instead of spreading out like oil is due to hydrogen bonding.
- The molecules "stick" to each other, resisting separation.
EPSPs Enable Neurons to Communicate and Transmit Signals
- EPSPs are the first step in transmitting signals across synapses.
- Without them, neurons couldn’t communicate with each other or with muscles and glands.
Key Points to Remember
- Neurotransmitter Release: Triggered by an action potential in the presynaptic neuron.
- Diffusion: Neurotransmitters cross the synaptic cleft by diffusion.
- Receptor Binding: Neurotransmitters bind to specific receptors on the postsynaptic membrane.
- Ion Flow: Binding opens ion channels, allowing ions to flow into the postsynaptic cell.
- EPSP Generation: The influx of ions changes the membrane potential, creating an EPSP.
Applications and Implications
- Understanding EPSPs has practical applications in medicine and pharmacology.
- For example, drugs that inhibit acetylcholinesterase are used to treat conditions like myasthenia gravis, a disorder that weakens muscles.
- How does the one-way transmission of signals across synapses relate to the concept of causality in Theory of Knowledge?
- Could this biological principle have broader implications in other fields?
- What would happen if acetylcholine were not broken down in the synaptic cleft?
- How might this affect muscle function?
- Can you explain how acetylcholine is broken down after it binds to its receptor? Why is this process important?
- How does acetylcholine contribute to the generation of an EPSP?


