Both receptor families sit on the same postsynaptic membrane and bind the same released neurotransmitter, but they convert that binding event into a signal on completely different timescales.
Ionotropic (ligand-gated channel):
dV/dt = -V/τ_f + Σ_pulses A_f · δ(t - t_release)
τ_f ≈ 2-4 ms → EPSP rises and decays within milliseconds
Metabotropic (GPCR → G-protein → adenylyl cyclase → cAMP):
dR/dt = k_on·L·(1-R) - k_off·R (receptor occupancy)
dC/dt = gain · R - C/τ_slow (cAMP accumulation)
τ_slow ≈ 0.2 - 2 s, gain ≈ 1-40 (catalytic amplification)
- Fire one pulse — releases a burst of vesicles from the presynaptic terminal; watch particles cross the cleft and split toward both receptor clusters.
- Ionotropic channel (blue, left) — the pore opens the instant a transmitter molecule binds and closes again within a few milliseconds. Fast, brief, not amplified: one molecule opens one channel.
- Metabotropic receptor (orange, right) — binding activates a G-protein, which activates adenylyl cyclase, which produces many cAMP molecules per activated receptor. The response ramps up slowly and lingers, but a single bound receptor triggers a cascade of thousands of downstream molecules — the "molecules amplified" readout tracks that gain.
- Auto-fire / rate slider — repeated pulses show temporal summation: the fast channel resets between spikes at high rates, while the slow cascade integrates and keeps climbing.
- Cascade gain / τ sliders — tune the catalytic amplification factor and the cAMP clearance rate, the two parameters that set how "loud" and how "sticky" a metabotropic response becomes.
Real synapses use this split deliberately: fast ionotropic transmission (e.g. AMPA/glutamate) carries moment-to-moment information, while slow metabotropic transmission (e.g. dopamine, serotonin, many neuropeptides) modulates excitability, mood and plasticity over seconds to minutes.