We are interested in the molecular basis of animal behavior. Behavior is the result of the function of excitable cells: neurons and muscles. We study excitable cell function in the nematode worm Caenorhabditis elegans (as well as other nematodes), where, because behavior is simple and the connections between electrical activity and behavior fairly direct, it is possible to make direct connections between specific molecules and the behaviors they influence. We concentrate specifically on the pharynx, a neuromuscular pump that is responsible for feeding behavior. The pharynx has 20 neurons of 14 different types and 20 muscle cells of 8 different types. Most of the projects in the lab fall into one of three general areas: electrophysiology, evolution of behavior, and regulation of feeding.
Pharyngeal electrophysiology, particularly the electrophysiology of the pharyngeal muscle, is the oldest and most developed of the subjects we study. The pharyngeal muscle is made of spontaneously active electrically coupled cells that are functionally similar to the cells of the vertebrate heart. We developed techniques for recording the electrical events in pharyngeal muscle, and by combining these techniques with forward and reverse genetics, we have identified the ion channels that shape the pharyngeal muscle action potential, and also the neurons that modulate feeding. We have recently discovered that dopamine and cocaine may modulate pharyngeal function. We’re keen to explore this as a possible model of addiction.
We are seeking to understand how behavior evolves by comparing feeding behavior and pharyngeal function in different nematode species. Interestingly, different nematodes, although they have different feeding behavior, have pharyngeal neurons and muscles cells that are structurally virtually identical. How do structurally identical nervous systems produce different behavior? We have evidence that synapses that work in one species may not work (or may work less well) in others. We are of course very interested in identifying the molecular and genetic bases for these differences in synaptic strength. We’ve identified one candidate: molecule, the Ca2+-activated K+ channel SLO-1.
I expect regulation of feeding to become our biggest area for research in the future. This subject may be significant for health because of its potential to help understand causes of the growing problem of human obesity. We have shown that worms regulate their feeding behavior similarly to humans. When starved, they become hungry and eat more -- we can now describe how this works in C elegans in molecular detail. Worms also discriminate between different foods: they prefer those that support growth and provide energy, just as most people prefer a cheeseburger to a carrot. Worms also become full: they stop eating and even appear to sleep when they have had too much food. Some of the molecular signals that mediate this response (insulin and neuropeptide Y) may be shared with humans.
RESEARCH INTERESTS
Neurobiology
Genetics
Caenorhabditis elegans
ion channels
feeding
RECENT PUBLICATIONS
Chiang, J-T, Steciuk, M, Shtonda, B, and Avery, L, "Evolution of pharyngeal behaviors and neuronal functions in free-living soil nematodes" Journal of Experimental Biology, 209:1859-1873, 2006
You, Y, Kim, J, Cobb, M, and Avery, L, "Starvation activates MAP Kinase through the muscarinic acetylcholine pathway in Caenorhabditis elegans pharynx" Cell Metabolism, 3:237-245, 2006
Shtonda, BB, and Avery, L, "Dietary choice behavior in Caenorhabditis elegans" Journal of Experimental Biology, 209:89-102, 2006
Shtonda, BB and Avery, L, "CCA-1, EGL-19 and EXP-2 currents shape action potentials in the Caenorhabditis elegans pharynx" Journal of Experimental Biology, 208:2177-2190, 2005
Steger, KA and Avery, L, "The GAR-3 muscarinic receptor cooperates with calcium signals to regulate muscle contraction in the C. elegans pharynx" Genetics, 167:633-643, 2004
SIGNIFICANT PUBLICATIONS
de Bono, M, Tobin, DM, Davis, MW, Avery, L, Bargmann, CI, "Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli" Nature, 419:899-903, 2002
Dent, JA, Smith, MM, Vassilatis, D, Avery, L, "Genetics of ivermectin resistance in C. elegans" Proc Natl Acad Sci USA, 97:2674-2679, 2000
Davis, MW, Fleischauer, R, Dent, JA, Joho, RH, Avery, L, "A Mutation in the C. elegans EXP-2 K+ Channel That Alters Feeding Behavior" Science, 286:2501-2504, 1999
Steger, KA, Shtonda, BB, Thacker, C, Snutch, TP, and Avery, L, "The C. elegans T-type calcium channel CCA-1 boosts neuromuscular transmission" Journal of Experimental Biology, 208:2191-2203, 2005
You, Y-J, Kim, J, Cobb, M, Avery, L, "Starvation activates MAP kinase through the muscarinic acetylcholine pathway in Caenorhabditis elegans pharynx" Cell Metabolism, 3:237-245, 2006
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