CO2 anesthesia (Henry Hickman Hill, 1823) is commonly used on a range of experimental animals from Drosophila through to rats despite having been dismissed as being 'Surgical Humbug' in the Lancet (http://www.sciencedirect.com/science/article/pii/S0140673602921835)! The mechanisms underlying CO2 anesthesia are remarkably poorly understood. A fall in CO2 (e.g. in hyperventilation) seems to produce the opposite effects to a rise, with general excitation being the most obvious symptom, yet the commonly held view that calcium buffering underlies the effect has not been supported by experimental evidence. Whilst some recent evidence suggests that pH changes may be involved our recent work (Caldwell et al., Synapse 2013) suggests an alternative mechanism. Altering CO2 levels has three direct effects - CO2 directly alters lipid fluidity and by reacting with water it alters pH and HCO3-. Each of these effects could alter membrane excitability. Over the last two months we have developed a novel technique to distinguish between these three effects using gaseous anesthesia in Drosophila. Using high throughput geotropic assays, the electroretinogram and neuromuscular junction we can observe the effects of H+, HCO3- and CO2 at the cellular, organ and whole animal level. By understanding how CO2 anesthesia occurs the project will also help our understanding of basic neuronal synaptic function.
- Antiquack (1826) Surgical Humbug. The Lancet, 5(127), 646 - 647.
- Caldwell et al. (2013). Presynaptic pH and vesicle fusion in Drosophila larvae neurones. Synapse 67, 729-740.
- Badre et al., (2005) The physiological and behavioral effects of carbon dioxide on Drosophila melanogaster larvae. Comparative Biochemistry and Physiology, 140, 363–376.