Abstract
Caenorhabditis elegans modulates its locomotory rate in response to its food, bacteria, in two ways. First, well-fed wild-type animals move more slowly in the presence of bacteria than in the absence of bacteria. This basal slowing response is mediated by a dopamine-containing neural circuit that senses a mechanical attribute of bacteria and may be an adaptive mechanism that increases the amount of time animals spend in the presence of food. Second, food-deprived wild-type animals, when transferred to bacteria, display a dramatically enhanced slowing response that ensures that the animals do not leave their newly encountered source of food. This experience-dependent response is mediated by serotonergic neurotransmission and is potentiated by fluoxetine (Prozac). The basal and enhanced slowing responses are distinct and separable neuromodulatory components of a genetically tractable paradigm of behavioral plasticity.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Caenorhabditis elegans / physiology*
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Caenorhabditis elegans Proteins*
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Catalase / genetics
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Dopamine / pharmacology
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Dopamine / physiology*
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Environment*
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Escherichia coli / physiology
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Fluoxetine / pharmacology
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Food Deprivation / physiology
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Fungal Proteins / genetics
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Helminth Proteins / genetics
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Mechanoreceptors / physiology
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Mixed Function Oxygenases*
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Motor Activity / drug effects
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Motor Activity / physiology*
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Mutation / physiology
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Neurons / physiology
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Selective Serotonin Reuptake Inhibitors / pharmacology
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Serotonin / physiology*
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Time Factors
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Trans-Activators / genetics
Substances
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Caenorhabditis elegans Proteins
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Fungal Proteins
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Helminth Proteins
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Serotonin Uptake Inhibitors
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Trans-Activators
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cat-2 protein, C elegans
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Fluoxetine
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Serotonin
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Mixed Function Oxygenases
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Catalase
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Dopamine