Neurotransmitter receptors on postsynaptic membranes control whether transmitter binding changes membrane potential or is blocked by antagonists, linking signal detection to a specific target-cell response.
Coverage 2022–2022 · Updated 15 Jul 2026
Acetylcholine binds a transmembrane receptor that is also a ligand-gated ion channel in the postsynaptic membrane.
Ligand binding changes the receptor's conformation and opens the channel. Positively charged ions diffuse into the postsynaptic cell down their electrochemical gradient, making the inside less negative and changing membrane potential.
Sequence: acetylcholine binds → receptor channel opens → positive ions enter → postsynaptic membrane depolarizes → the voltage change may trigger further events.
At a cholinergic synapse, opening acetylcholine-receptor channels produces a local depolarization; if combined depolarization reaches threshold, a postsynaptic action potential can follow.
Acetylcholine does not itself cross the membrane or carry charge into the cell. It opens a receptor channel; ion diffusion causes the voltage change.
This objective is assessed through multiple choice.
Build the answer around this relationship: Neurotransmitters bind receptors on the postsynaptic membrane.
Representative question
Atropine drops are used by opticians to dilate the pupil, so that a thorough examination of the retina can be performed. Atropine binds to acetylcholine receptors in synapses.
What is the effect of atropine binding in synapses?
Inhibits the binding of acetylcholine at the presynaptic membrane
Inhibits the release of acetylcholine from the presynaptic neuron
Prevents binding of acetylcholine at the postsynaptic membrane
Prevents transport of acetylcholine through the postsynaptic membrane
A ligand only affects target cells with the matching receptor. Quorum sensing uses autoinducers and thresholds for group behaviour. Animal signals differ by source, distance, speed, target-cell response, and chemical class. Hydrophilic ligands use transmembrane receptors and relays; steroid and thyroid hormones use intracellular receptors that affect transcription. Named pathways then show the logic: acetylcholine opens sodium channels, GPCRs switch G proteins through GDP-GTP exchange, epinephrine uses cAMP and kinase cascades, insulin RTKs use dimerisation/autophosphorylation to move GLUT4 and promote glycogenesis, steroid hormones change gene expression, and feedback either amplifies or restores stability.
