I have pondered possible mechanism of anesthesia in TGD framework several times earlier (see this and this) and it is interesting to see whether the findings allow to make earlier insights more detailed or even develop new ones.
What was observed
According to the popular article the discovery by chemist Richard Lerner, MD, and molecular biologist Scott Hansen, PhD, settles a century-old scientific debate about whether anesthetics act directly on cell-membrane gates called ion channels, or do they somehow act on the membrane to signal cell changes in a new and unexpected way. The conclusion of the researcheres is that anesthetic action is a two-step process that begins in the membrane. The anesthetics perturb ordered lipid clusters within the cell membrane known as "lipid rafts" to initiate the signal. There are two kinds of clusters involved and known with names GM1 and PIP2.
What was observed was following.
- A shift in the GM1 cluster’s organization, a shift from a tightly packed ball to a disrupted mess occurred first As GM1 grew disordered, it spilled its contents, among them, an enzyme called phospholipase D2 (PLD2). Melting is a good analog for what happens. Gel-to-sol transition in cytoplasm is second analogy.
- PLD2 moved like a billiard ball away from its GM1 home and over to a different, less-preferred lipid cluster called PIP2.
- This activates key molecules within PIP2 clusters, TREK1 potassium ion channels and their lipid activator, phosphatidic acid (PA) are among them. The activation of TREK1 potassium channels releases potassium hyper-polarizing the nerve and it makes it more difficult to fire. Nerve pulse generation rate becomes low and leads to a loss of consciousness - at least in clinical sense. Something analogous to this could happen when one falls in sleep.
See the article TGD interpretation of new experimental results about the mechanism of anesthesia or the chapter TGD Inspired Model for Nerve Pulse.
For a summary of earlier postings see Latest progress in TGD.