Every message between neurons crosses a tiny gap — the synapse. The sending cell squirts neurotransmitter into the cleft; it drifts across and binds receptors on the far side, and each bound receptor nudges the receiving cell toward firing. Then transporters vacuum the transmitter back up — reuptake — and the signal switches off.
A drug can hijack any one step. An agonist is a copycat key: it binds and fires the receptor itself, no neuron needed. An antagonist plugs the receptor so the real transmitter is locked out. A reuptake inhibitor jams the vacuum, so transmitter lingers and the signal piles up. Three different molecular tricks — one dial, the receiving cell's firing rate, turned up or down.
Under the hood is textbook mass-action receptor kinetics: transmitter and drug compete for a shared pool of receptors with fixed on/off rates, and reuptake sets how fast the cleft clears. Nothing is scripted — the agonist, antagonist and inhibitor are just three edits to the same rate equations. The dashed gold marks show where occupancy and firing are heading for your current settings. The concentrations are illustrative, tuned to the lesson.
Something in the simulation stopped unexpectedly — the lesson continues without it. You can move on; nothing you did was wrong.