Pathogenic bacteria induce aversive olfactory learning in Caenorhabditis elegans

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 mal...

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Veröffentlicht in:Nature 2005-11, Vol.438 (7065), p.179-184
Hauptverfasser: Zhang, Yun, Lu, Hang, Bargmann, Cornelia I.
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Sprache:eng
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Zusammenfassung: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. They smell trouble In the wild, the lifespan of the Caenorhabditis elegans worm, a common lab model in studies of neurobiology, genetics and longevity, may be limited by pathogenic infection by soil bacteria. Now a previously unknown mechanism by which C. elegans avoids these pathogens has been discovered: it detects the odour of the bacteria, and via activation of specific neurons that upregulate the modulatory neurotransmitter serotonin, it learns to associate the odour with a hazard. The results suggest that the role of serotonin in signalling intestinal malaise may be primitive and conserved in animals, since in mammals serotonin receptors are major targets of antinausea drugs.
ISSN:0028-0836
1476-4687
1476-4679
DOI:10.1038/nature04216