Ca2+ signaling via the neuronal calcium sensor-1 regulates associative learning and memory in C. elegans

• Published in: Neuron (Cambridge, Mass.) Mass.), 2001-04, Vol.30 (1), p.241-248
• Main Authors: Gomez, M, De Castro, E, Guarin, E, Sasakura, H, Kuhara, A, Mori, I, Bartfai, T, Bargmann, C I, Nef, P
• Format: Article
• Language: English
• Subjects: Animals; Behavior, Animal - physiology; Caenorhabditis elegans - cytology; Caenorhabditis elegans - metabolism; Calcium Signaling - physiology; Calcium-Binding Proteins - genetics; Calcium-Binding Proteins - metabolism; Feeding Behavior - physiology; Gene Expression Regulation - physiology; Learning - physiology; Memory - physiology; Mutation - physiology; Nervous System - cytology; Nervous System - metabolism; Neural Pathways - cytology; Neural Pathways - metabolism; Neuronal Calcium-Sensor Proteins; Neurons - cytology; Neurons - metabolism; Neuropeptides - genetics; Neuropeptides - metabolism; Synaptic Transmission - physiology; Thermosensing - genetics
• ISSN: 0896-6273
• DOI: 10.1016/s0896-6273(01)00276-8

On a radial temperature gradient, C. elegans worms migrate, after conditioning with food, toward their cultivation temperature and move along this isotherm. This experience-dependent behavior is called isothermal tracking (IT). Here we show that the neuron-specific calcium sensor-1 (NCS-1) is essential for optimal IT. ncs-1 knockout animals show major defects in IT behavior, although their chemotactic, locomotor, and thermal avoidance behaviors are normal. The knockout phenotype can be rescued by reintroducing wild-type NCS-1 into the AIY interneuron, a key component of the thermotaxis network. A loss-of-function form of NCS-1 incapable of binding calcium does not restore IT, whereas NCS-1 overexpression enhances IT performance levels, accelerates learning (faster acquisition), and produces a memory with slower extinction. Thus, proper calcium signaling via NCS-1 defines a novel pathway essential for associative learning and memory.