The presynaptic terminal releases neurotransmitter (teal) into the synaptic cleft at a steady rate; reuptake pumps on the presynaptic membrane clear it back out. Postsynaptic receptors activate when bound by transmitter, driving the "activation" reading.
An agonist (violet) mimics the transmitter and binds receptors directly, adding to activation on top of whatever the natural transmitter is doing. An antagonist occupies receptors without activating them, blocking the transmitter from binding there — activation drops even though release is unchanged. A reuptake inhibitor jams the presynaptic pumps instead of touching receptors, so transmitter lingers in the cleft and keeps activating receptors for longer — the SSRI mechanism.
activation ∝ sensitivity · bound_receptors / total
sensitivity -= k_down · max(0, activation − threshold) · dt
sensitivity += k_up · (1 − sensitivity) · dt
- Dose — how much drug is present in the cleft; higher dose means more receptor sites (or pumps) occupied per second.
- Sensitivity — represents receptor density/responsiveness. Hold activation high for long enough and receptors desensitize (downregulate), the real basis of pharmacological tolerance; drop activation and sensitivity slowly recovers.
This is a didactic, not clinical, model — real synapses involve dozens of receptor subtypes, second-messenger cascades and diffusion geometry this simulator does not attempt to capture.