@article {Bargmann:2006kx,
	title = {Chemosensation in C. elegans.},
	journal = {WormBook},
	year = {2006},
	pages = {1{\textendash}29},
	address = {Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. cori@rockefeller.edu},
	abstract = {C. elegans has a highly developed chemosensory system that enables it to detect a wide variety of volatile (olfactory) and water-soluble (gustatory) cues associated with food, danger, or other animals. Much of its nervous system and more than 5\% of its genes are devoted to the recognition of environmental chemicals. Chemosensory cues can elicit chemotaxis, rapid avoidance, changes in overall motility, and entry into and exit from the alternative dauer developmental stage. These behaviors are regulated primarily by the amphid chemosensory organs, which contain eleven pairs of chemosensory neurons. Each amphid sensory neuron expresses a specific set of candidate receptor genes and detects a characteristic set of attractants, repellents, or pheromones. About 500-1000 different G protein-coupled receptors (GPCRs) are expressed in chemosensory neurons, and these may be supplemented by alternative sensory pathways as well. Downstream of the GPCRs, two signal transduction systems are prominent in chemosensation, one that uses cGMP as a second messenger to open cGMP-gated channels, and one that relies upon TRPV channels. These sensory pathways are modulated and fine-tuned by kinases and phosphatases. Chemosensory preferences can be modified by sensory adaptation, developmental history, and associative learning, allowing C. elegans to integrate context and experience into its behavior.},
	issn = {1551-8507 (Electronic)},
	doi = {10.1895/wormbook.1.123.1},
	author = {Bargmann, Cornelia I}
}
@article {Zhang:2005ws,
	title = {Pathogenic bacteria induce aversive olfactory learning in Caenorhabditis elegans.},
	journal = {Nature},
	volume = {438},
	number = {7065},
	year = {2005},
	pages = {179{\textendash}184},
	address = {Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University, New York, New York 10021, USA.},
	abstract = {Food can be hazardous, either through toxicity or through bacterial infections that follow the ingestion of a tainted food source. Because learning about food quality enhances survival, one of the most robust forms of olfactory learning is conditioned avoidance of tastes associated with visceral malaise. The nematode Caenorhabditis elegans feeds on bacteria but is susceptible to infection by pathogenic bacteria in its natural environment. Here we show that C. elegans modifies its olfactory preferences after exposure to pathogenic bacteria, avoiding odours from the pathogen and increasing its attraction to odours from familiar nonpathogenic bacteria. Particular bacteria elicit specific changes in olfactory preferences that are suggestive of associative learning. Exposure to pathogenic bacteria increases serotonin in ADF chemosensory neurons by transcriptional and post-transcriptional mechanisms. Serotonin functions through MOD-1, a serotonin-gated chloride channel expressed in sensory interneurons, to promote aversive learning. An increase in serotonin may represent the negative reinforcing stimulus in pathogenic infection.},
	issn = {1476-4687 (Electronic)},
	doi = {10.1038/nature04216},
	author = {Zhang, Yun and Lu, Hang and Bargmann, Cornelia I}
}
