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.
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