Induced changes in protein receptors conferring resistance to anesthetics

Although general anesthetics have been provided effectively for many years, their exact molecular underpinnings remain relatively unknown. In this article, we discuss the recent findings associated with resistance to anesthetic effects as a way of shedding light on these mechanisms.

The original theories of anesthetic action based upon their effects on cellular membranes have given way to specific theories concerning direct effects on ion channel proteins. These molecular targets are intimately involved in the conduct of neuronal signaling within the central nervous system and are thought to be essential in the modulation of conscious states. It is the lack of a thorough understanding of unperturbed consciousness that fosters great difficulty in understanding how anesthetics alter this conscious state. However, one very fruitful line of analysis in the quest for such answers lies in the examination of both in-vitro and in-vivo ion channel systems that seem to maintain variable levels of resistance to anesthetics.

Information about the possible targets and molecular nature of anesthetic action is being derived from studies of anesthetic resistance in γ aminobutyric acid receptors, tandem pore potassium channels, and an apparently wide variety of protein systems within the nematode, Caenorhabditis elegans.