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      A Hub-and-Spoke Circuit Drives Pheromone Attraction and Social Behavior in C. elegans

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Innate social behaviors emerge from neuronal circuits that interpret sensory information based on an individual's own genotype, sex, and experience. The regulated aggregation behavior of C. elegans, a simple animal with only 302 neurons, is an attractive system to analyze these circuits. Wild social strains of the nematode Caenorhabditis elegans aggregate in the presence of specific sensory cues, but solitary strains do not 1, 2, 3, 4. Here we identify the RMG inter/motor neuron as the hub of a regulated circuit that controls aggregation and related behaviors. RMG is the central site of action of the neuropeptide receptor gene npr-1, which distinguishes solitary strains (high npr-1 activity) from wild social strains (low npr-1 activity); high RMG activity is essential for all aspects of social behavior. Anatomical gap junctions connect RMG to multiple classes of sensory neurons known to promote aggregation, and to ASK sensory neurons, which are implicated in male attraction to hermaphrodite pheromones 5. We find that ASK neurons respond directly to pheromones, and that high RMG activity enhances ASK responses in social strains, causing hermaphrodite attraction to pheromones at concentrations that repel solitary hermaphrodites. The coordination of social behaviors by RMG suggests an anatomical hub-and-spoke model for sensory integration in aggregation, and points to functions for related circuit motifs in the C. elegans wiring diagram.

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          Most cited references 25

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          A high signal-to-noise Ca(2+) probe composed of a single green fluorescent protein.

           J Nakai,  M Ohkura,  K Imoto (2001)
          Recently, several groups have developed green fluorescent protein (GFP)-based Ca(2+) probes. When applied in cells, however, these probes are difficult to use because of a low signal-to-noise ratio. Here we report the development of a high-affinity Ca(2+) probe composed of a single GFP (named G-CaMP). G-CaMP showed an apparent K(d) for Ca(2+) of 235 nM. Association kinetics of Ca(2+) binding were faster at higher Ca(2+) concentrations, with time constants decreasing from 230 ms at 0.2 microM Ca(2+) to 2.5 ms at 1 microM Ca(2+). Dissociation kinetics (tau approximately 200 ms) are independent of Ca(2+) concentrations. In HEK-293 cells and mouse myotubes expressing G-CaMP, large fluorescent changes were observed in response to application of drugs or electrical stimulations. G-CaMP will be a useful tool for visualizing intracellular Ca2+ in living cells. Mutational analysis, together with previous structural information, suggests the residues that may alter the fluorescence of GFP.
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            Wiring optimization can relate neuronal structure and function.

            We pursue the hypothesis that neuronal placement in animals minimizes wiring costs for given functional constraints, as specified by synaptic connectivity. Using a newly compiled version of the Caenorhabditis elegans wiring diagram, we solve for the optimal layout of 279 nonpharyngeal neurons. In the optimal layout, most neurons are located close to their actual positions, suggesting that wiring minimization is an important factor. Yet some neurons exhibit strong deviations from "optimal" position. We propose that biological factors relating to axonal guidance and command neuron functions contribute to these deviations. We capture these factors by proposing a modified wiring cost function.
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              Dissecting a circuit for olfactory behaviour in Caenorhabditis elegans.

              Although many properties of the nervous system are shared among animals and systems, it is not known whether different neuronal circuits use common strategies to guide behaviour. Here we characterize information processing by Caenorhabditis elegans olfactory neurons (AWC) and interneurons (AIB and AIY) that control food- and odour-evoked behaviours. Using calcium imaging and mutations that affect specific neuronal connections, we show that AWC neurons are activated by odour removal and activate the AIB interneurons through AMPA-type glutamate receptors. The level of calcium in AIB interneurons is elevated for several minutes after odour removal, a neuronal correlate to the prolonged behavioural response to odour withdrawal. The AWC neuron inhibits AIY interneurons through glutamate-gated chloride channels; odour presentation relieves this inhibition and results in activation of AIY interneurons. The opposite regulation of AIY and AIB interneurons generates a coordinated behavioural response. Information processing by this circuit resembles information flow from vertebrate photoreceptors to 'OFF' bipolar and 'ON' bipolar neurons, indicating a conserved or convergent strategy for sensory information processing.
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                Author and article information

                Journal
                0410462
                6011
                Nature
                Nature
                0028-0836
                1476-4687
                1 April 2009
                6 April 2009
                30 April 2009
                30 October 2009
                : 458
                : 7242
                : 1171-1175
                Affiliations
                [1 ]Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University, 1230 York Avenue, New York, NY 10065
                [2 ]Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115
                Author notes

                Author contributions

                CIB is an Investigator of the Howard Hughes Medical Institute. EZM performed experiments; NP, EHF, SC, RAB, and JC developed experimental methods and reagents; EZM and CIB designed and interpreted experiments and wrote the paper.

                Article
                nihpa102697
                10.1038/nature07886
                2760495
                19349961
                Funding
                Funded by: National Institute of General Medical Sciences : NIGMS
                Funded by: National Cancer Institute : NCI
                Funded by: Howard Hughes Medical Institute
                Award ID: T32 GM007739-30 ||GM
                Funded by: National Institute of General Medical Sciences : NIGMS
                Funded by: National Cancer Institute : NCI
                Funded by: Howard Hughes Medical Institute
                Award ID: R01 CA024487-30 ||CA
                Funded by: National Institute of General Medical Sciences : NIGMS
                Funded by: National Cancer Institute : NCI
                Funded by: Howard Hughes Medical Institute
                Award ID: F32 GM077943-03 ||GM
                Funded by: National Institute of General Medical Sciences : NIGMS
                Funded by: National Cancer Institute : NCI
                Funded by: Howard Hughes Medical Institute
                Award ID: ||HHMI_
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