Meyer-Overton tells us that all anesthetics act on the same target (a protein). Many but not all anesthetics bind GABA_A inhibitory receptors, but some open them and some close them.
Same with other membrane receptors and channels. Microtubule tubulin proteins appear to bind all anesthetics though low affinity compared to GABA_A receptor binding. But there are about a million more tubulins per neuron than GABA_A receptors. And they’re in a quantum condensate so decohering any part would disrupt the whole.
Ignoring Meyer -Overton is like ignoring the Rosetta Stone if you’re trying to understand ancient Sumerian.
And thalamus can’t be necessary for consciousness because conscious smell doesnt go through thalamus.
Anesthetics hit GABA_A/glycine/NMDA channels at the synapse — that part's settled pharmacology, not in dispute. What that does functionally is decouple the thalamocortical loop from proprioceptive-vestibular afference: cortex stops integrating the ongoing P-V return signal even though the signal itself (muscle spindle, GTO, otolithic, canal input) is still arriving. Occurrence, on this account, isn't a property generated inside tubulin — it's what happens when a return operator ℛ keeps regulating the α/θ ratio ρ against a live proprioceptive-vestibular reference. Cut the cortical side out of that loop and ρ has nothing left to regulate. α/θ collapses or flattens not because a quantum process in the cytoskeleton switched off, but because the regulatory loop generating that spectral signature no longer has an input to close around.
That's why anesthesia, sleep, and Ian Waterman’s kind of deafferentation all show family-resemblant EEG signatures without needing a shared molecular substrate — they're different ways of breaking the same loop (cortical gating vs. loss of the input itself), not different doses of the same microtubule effect.
Sep 23, 2026 · 3:27 AM UTC
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