A new study suggests that the answer to this age-old question may lie in the effect of anesthesia on the organization of lipids in the cell's outer membrane, potentially altering the ability to send signals along nerve cells.

Researchers at the US National Institute of Standards and Technology (NIST; Gaithersburg, MD, USA) set out to find out how exactly inhaled anesthetics interact with protein ion channels--large proteins embedded in the relatively small lipid molecules forming the membrane--which are responsible for conducting electrical impulses along the myelin sheath of the nerve cells. They found that while a cell membrane is a highly fluid film made of many different kinds of lipid molecules, the region immediately surrounding an ion channel often consists of a single type of lipids that form a sort of "raft" that is more ordered and less fluid then the rest of the membrane.

When prior research demonstrated that disrupting these lipid rafts could affect a channel's function, the researchers conducted X-ray and neutron diffraction studies of a binary lipid membrane that demonstrated that halothane (at physiological concentrations) produces a pronounced redistribution of lipids between domains of different lipid types, as identified by different lamellar d-spacing and isotope composition. In contrast, dichlorohexafluorocyclobutane (F6), a halogenated nonanesthetic, does not produce such significant effects. According to the researchers, these findings demonstrate a specific effect of inhalational anesthetics on mixing phase equilibria of a lipid mixture. The study was published on February 21, 2012, in Langmuir.

“A better fundamental understanding of inhaled anesthetics could allow us to design better ones with fewer side effects,” concluded lead author Hirsh Nanda, PhD, and colleagues of the NIST Center for Neutron Research (NCNR). “How these chemicals work in the body is a scientific mystery that stretches back to the Civil War.”

Related Links:
US National Institute of Standards and Technology