Diethyl ether, first demonstrated publicly at Massachusetts General Hospital's "Ether Dome" in 1846, does not numb tissue directly — it crosses the blood-brain barrier and binds the GABA-A receptor, a chloride channel on neurons. Bound receptor fraction follows a Hill equation:
occupancy(C) = C^n / (EC50^n + C^n), n = 2
g_GABA = g_max · occupancy(C)
The soma is a spiking Izhikevich neuron with the GABA-A channel added as a shunting chloride conductance toward E_Cl = -70 mV:
v' = 0.04v² + 5v + 140 − u + I − g_GABA·(v − E_Cl)
u' = a·(b·v − u)
if v ≥ 30 mV: v ← c, u ← u + d
As ether concentration C rises, g_GABA grows and clamps v toward -70 mV faster than the stimulus current I can depolarize it to threshold. The neuron stops firing, no action potential is launched, and the traveling pulse on the axon disappears — the cellular basis of surgical anesthesia. Because the shunt divides the depolarizing drive rather than subtracting from it, conduction can actually block well below the nominal EC50 once I is small — the same steep, patient-specific threshold anesthesiologists target with MAC dosing (reproduced here exactly as computed, not rounded to look tidier).
- Ether concentration — sets C directly; drag it or use Induce/Wake up to ramp it automatically over ~15s.
- Stimulus current I — the excitatory drive reaching the soma (pain signal, touch, etc.); higher I needs more ether to suppress.
- Patient sensitivity (EC50) — individual variability in anesthetic requirement, exactly like real MAC differing between patients. Watch the dose-response curve panel shift as you drag it.
- Axon panel — drag to pan along the axon, scroll/pinch or use +/− to zoom; the traveling action potential (teal) is the thing anesthesia extinguishes.