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  • 1
    Publication Date: 2009-04-08
    Description: Innate social behaviours emerge from neuronal circuits that interpret sensory information on the basis of an individual's own genotype, sex and experience. The regulated aggregation behaviour of the nematode Caenorhabditis elegans, a simple animal with only 302 neurons, is an attractive system to analyse these circuits. Wild social strains of C. elegans aggregate in the presence of specific sensory cues, but solitary strains do not. Here we identify the RMG inter/motor neuron as the hub of a regulated circuit that controls aggregation and related behaviours. 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 behaviour. Anatomical gap junctions connect RMG to several classes of sensory neurons known to promote aggregation, and to ASK sensory neurons, which are implicated in male attraction to hermaphrodite pheromones. 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 behaviours 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.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760495/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2760495/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Macosko, Evan Z -- Pokala, Navin -- Feinberg, Evan H -- Chalasani, Sreekanth H -- Butcher, Rebecca A -- Clardy, Jon -- Bargmann, Cornelia I -- CA24487/CA/NCI NIH HHS/ -- F32 GM077943/GM/NIGMS NIH HHS/ -- F32 GM077943-03/GM/NIGMS NIH HHS/ -- GM07739/GM/NIGMS NIH HHS/ -- GM077943/GM/NIGMS NIH HHS/ -- R01 CA024487/CA/NCI NIH HHS/ -- R01 CA024487-30/CA/NCI NIH HHS/ -- T32 GM007739/GM/NIGMS NIH HHS/ -- T32 GM007739-30/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Apr 30;458(7242):1171-5. doi: 10.1038/nature07886. Epub 2009 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University, 1230 York Avenue, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19349961" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/cytology/drug effects/*physiology ; Caenorhabditis elegans Proteins/genetics/metabolism ; Disorders of Sex Development ; Feeding Behavior/drug effects/physiology ; Male ; Models, Neurological ; Mutation ; Neural Pathways/drug effects/*physiology ; Neurons/drug effects/physiology ; Pheromones/pharmacology/*physiology ; Receptors, Neuropeptide Y/genetics/metabolism ; *Social Behavior
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-03-08
    Description: Larval development of the nematode Caenorhabditis elegans is controlled by the activities of four classes of chemosensory neurons. The choice between normal development and development into a specialized larval form called a dauer larva is regulated by competing environmental stimuli: food and a dauer pheromone. When the neuron classes ADF, ASG, ASI, and ASJ are killed, animals develop as dauer larvae regardless of environmental conditions. These neurons might sense food or dauer pheromone, or both, to initiate the specialized differentiation of many cell types that occurs during dauer formation. Entry into and exit from the dauer stage are primarily controlled by different chemosensory neurons. The analysis of mutants defective in dauer formation indicates that the chemosensory neurons are active in the absence of sensory inputs and that dauer pheromone inhibits the ability of these neurons to generate a signal necessary for normal development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bargmann, C I -- Horvitz, H R -- GM24663/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1991 Mar 8;251(4998):1243-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2006412" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis/*growth & development ; Cell Survival ; Larva ; Models, Neurological ; Mutation ; Neurons, Afferent/cytology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2008-09-20
    Description: A large body of evidence indicates that metazoan innate immunity is regulated by the nervous system, but the mechanisms involved in the process and the biological importance of such control remain unclear. We show that a neural circuit involving npr-1, which encodes a G protein-coupled receptor (GPCR) related to mammalian neuropeptide Y receptors, functions to suppress innate immune responses. The immune inhibitory function requires a guanosine 3',5'-monophosphate-gated ion channel encoded by tax-2 and tax-4 as well as the soluble guanylate cyclase GCY-35. Furthermore, we show that npr-1- and gcy-35-expressing sensory neurons actively suppress immune responses of nonneuronal tissues. A full-genome microarray analysis on animals with altered neural function due to mutation in npr-1 shows an enrichment in genes that are markers of innate immune responses, including those regulated by a conserved PMK-1/p38 mitogen-activated protein kinase signaling pathway. These results present evidence that neurons directly control innate immunity in C. elegans, suggesting that GPCRs may participate in neural circuits that receive inputs from either pathogens or infected sites and integrate them to coordinate appropriate immune responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831475/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831475/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Styer, Katie L -- Singh, Varsha -- Macosko, Evan -- Steele, Sarah E -- Bargmann, Cornelia I -- Aballay, Alejandro -- GM070977/GM/NIGMS NIH HHS/ -- R01 GM070977/GM/NIGMS NIH HHS/ -- R01 GM070977-01A1/GM/NIGMS NIH HHS/ -- U54 AI057157/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Oct 17;322(5900):460-4. doi: 10.1126/science.1163673. Epub 2008 Sep 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18801967" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/genetics/*immunology/microbiology/physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; Enterococcus faecalis/immunology/pathogenicity ; Gene Expression Regulation ; Genes, Helminth ; Guanylate Cyclase/genetics/metabolism ; *Immunity, Innate ; Ion Channels/genetics/metabolism ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinases/genetics/metabolism ; Mutation ; Nerve Net/physiology ; Neurons, Afferent/*metabolism ; Oligonucleotide Array Sequence Analysis ; Oxygen/physiology ; Pseudomonas aeruginosa/immunology/pathogenicity ; Receptors, Neuropeptide Y/genetics/*metabolism ; Salmonella enterica/immunology/pathogenicity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2012-11-01
    Description: Many biological functions are conserved, but the extent to which conservation applies to integrative behaviors is unknown. Vasopressin and oxytocin neuropeptides are strongly implicated in mammalian reproductive and social behaviors, yet rodent loss-of-function mutants have relatively subtle behavioral defects. Here we identify an oxytocin/vasopressin-like signaling system in Caenorhabditis elegans, consisting of a peptide and two receptors that are expressed in sexually dimorphic patterns. Males lacking the peptide or its receptors perform poorly in reproductive behaviors, including mate search, mate recognition, and mating, but other sensorimotor behaviors are intact. Quantitative analysis indicates that mating motor patterns are fragmented and inefficient in mutants, suggesting that oxytocin/vasopressin peptides increase the coherence of mating behaviors. These results indicate that conserved molecules coordinate diverse behavioral motifs in reproductive behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597094/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3597094/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garrison, Jennifer L -- Macosko, Evan Z -- Bernstein, Samantha -- Pokala, Navin -- Albrecht, Dirk R -- Bargmann, Cornelia I -- GM07739/GM/NIGMS NIH HHS/ -- K99 GM092859/GM/NIGMS NIH HHS/ -- K99GM092859/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 26;338(6106):540-3. doi: 10.1126/science.1226201.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Lulu and Anthony Wang Laboratory of Neural Circuits and Behavior, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23112335" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; *Biological Evolution ; CHO Cells ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans ; Proteins/agonists/chemistry/genetics/pharmacology/*physiology ; Cricetinae ; Humans ; Male ; Neuropeptides/chemistry/genetics/pharmacology/*physiology ; Oxytocin/chemistry/genetics/pharmacology/*physiology ; Receptors, G-Protein-Coupled/agonists/genetics/*physiology ; Reproduction ; Sexual Behavior, Animal/*physiology ; Vasopressins/chemistry/genetics/pharmacology/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-12-16
    Description: Neurotransmitter receptors, neurotransmitter synthesis and release pathways, and heterotrimeric GTP-binding protein (G protein)-coupled second messenger pathways are highly conserved between Caenorhabditis elegans and mammals, but gap junctions and chemosensory receptors have independent origins in vertebrates and nematodes. Most ion channels are similar to vertebrate channels but there are no predicted voltage-activated sodium channels. The C. elegans genome encodes at least 80 potassium channels, 90 neurotransmitter-gated ion channels, 50 peptide receptors, and up to 1000 orphan receptors that may be chemoreceptors. For many gene families, C. elegans has both conventional members and divergent outliers with weak homology to known genes; these outliers may provide insights into previously unknown functions of conserved protein families.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bargmann, C I -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2028-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Programs in Developmental Biology, Neuroscience, and Genetics, Department of Anatomy, University of California, San Francisco, CA 94143-0452, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851919" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*genetics/physiology ; GTP-Binding Proteins/genetics/metabolism ; Gap Junctions/genetics/physiology ; *Genes, Helminth ; Genome ; Ion Channels/genetics/physiology ; *Nervous System Physiological Phenomena ; Neuronal Plasticity ; Neurons/metabolism ; Neurotransmitter Agents/genetics ; Receptors, Cell Surface/genetics/metabolism ; Sensory Receptor Cells/metabolism ; Synapses/physiology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2004-07-03
    Description: During axon guidance, the ventral guidance of the Caenorhabditis elegans anterior ventral microtubule axon is controlled by two cues, the UNC-6/netrin attractant recognized by the UNC-40/DCC receptor and the SLT-1/slit repellent recognized by the SAX-3/robo receptor. We show here that loss-of-function mutations in clr-1 enhance netrin-dependent attraction, suppressing ventral guidance defects in slt-1 mutants. clr-1 encodes a transmembrane receptor protein tyrosine phosphatase (RPTP) that functions in AVM to inhibit signaling through the DCC family receptor UNC-40 and its effector, UNC-34/enabled. The known effects of other RPTPs in axon guidance could result from modulation of guidance receptors like UNC-40/DCC.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chang, Chieh -- Yu, Timothy W -- Bargmann, Cornelia I -- Tessier-Lavigne, Marc -- New York, N.Y. -- Science. 2004 Jul 2;305(5680):103-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Howard Hughes Medical Institute (HHMI), Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15232111" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Animals, Genetically Modified ; Axons/*physiology ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/chemistry/*genetics/*metabolism ; Cell Adhesion Molecules/genetics/metabolism ; Cell Movement ; Cues ; Genes, Helminth ; Microtubules/physiology/ultrastructure ; Models, Biological ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/genetics/*metabolism ; Open Reading Frames ; Phenotype ; Protein Tyrosine Phosphatases/chemistry/*genetics/*metabolism ; Receptor-Like Protein Tyrosine Phosphatases ; Receptors, Immunologic/metabolism ; Signal Transduction
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2011-03-18
    Description: Innate behaviours are flexible: they change rapidly in response to transient environmental conditions, and are modified slowly by changes in the genome. A classical flexible behaviour is the exploration-exploitation decision, which describes the time at which foraging animals choose to abandon a depleting food supply. We have used quantitative genetic analysis to examine the decision to leave a food patch in Caenorhabditis elegans. Here we show that patch-leaving is a multigenic trait regulated in part by naturally occurring non-coding polymorphisms in tyra-3 (tyramine receptor 3), which encodes a G-protein-coupled catecholamine receptor related to vertebrate adrenergic receptors. tyra-3 acts in sensory neurons that detect environmental cues, suggesting that the internal catecholamines detected by tyra-3 regulate responses to external conditions. These results indicate that genetic variation and environmental cues converge on common circuits to regulate behaviour, and suggest that catecholamines have an ancient role in regulating behavioural decisions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154120/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154120/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bendesky, Andres -- Tsunozaki, Makoto -- Rockman, Matthew V -- Kruglyak, Leonid -- Bargmann, Cornelia I -- GM089972/GM/NIGMS NIH HHS/ -- R01 GM089972/GM/NIGMS NIH HHS/ -- R01 GM089972-02/GM/NIGMS NIH HHS/ -- R01 HG004321/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 21;472(7343):313-8. doi: 10.1038/nature09821. Epub 2011 Mar 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21412235" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Behavior, Animal/*physiology ; Caenorhabditis elegans/classification/*genetics/*physiology ; Caenorhabditis elegans Proteins/*genetics/metabolism ; Catecholamines/metabolism ; Decision Making/physiology ; Environment ; Feeding Behavior/*physiology ; Gene Expression Regulation ; Multifactorial Inheritance/genetics ; Polymorphism, Genetic/*genetics ; Quantitative Trait Loci/genetics ; Receptors, Catecholamine/*genetics/metabolism ; Sensory Receptor Cells/metabolism ; Time Factors ; Tyramine/metabolism
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  • 8
    Publication Date: 2011-08-19
    Description: Evolution can follow predictable genetic trajectories, indicating that discrete environmental shifts can select for reproducible genetic changes. Conspecific individuals are an important feature of an animal's environment, and a potential source of selective pressures. Here we show that adaptation of two Caenorhabditis species to growth at high density, a feature common to domestic environments, occurs by reproducible genetic changes to pheromone receptor genes. Chemical communication through pheromones that accumulate during high-density growth causes young nematode larvae to enter the long-lived but non-reproductive dauer stage. Two strains of Caenorhabditis elegans grown at high density have independently acquired multigenic resistance to pheromone-induced dauer formation. In each strain, resistance to the pheromone ascaroside C3 results from a deletion that disrupts the adjacent chemoreceptor genes serpentine receptor class g (srg)-36 and -37. Through misexpression experiments, we show that these genes encode redundant G-protein-coupled receptors for ascaroside C3. Multigenic resistance to dauer formation has also arisen in high-density cultures of a different nematode species, Caenorhabditis briggsae, resulting in part from deletion of an srg gene paralogous to srg-36 and srg-37. These results demonstrate rapid remodelling of the chemoreceptor repertoire as an adaptation to specific environments, and indicate that parallel changes to a common genetic substrate can affect life-history traits across species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257054/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257054/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGrath, Patrick T -- Xu, Yifan -- Ailion, Michael -- Garrison, Jennifer L -- Butcher, Rebecca A -- Bargmann, Cornelia I -- GM07739/GM/NIGMS NIH HHS/ -- K99 GM092859/GM/NIGMS NIH HHS/ -- K99 GM092859-02/GM/NIGMS NIH HHS/ -- R00 GM087533/GM/NIGMS NIH HHS/ -- R00GM87533/GM/NIGMS NIH HHS/ -- T32 GM007739/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Aug 17;477(7364):321-5. doi: 10.1038/nature10378.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Neural Circuits and Behavior, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21849976" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological/genetics/physiology ; Animals ; *Biological Evolution ; Caenorhabditis elegans/classification/drug effects/*genetics/*physiology ; Environment ; Evolution, Molecular ; Glycolipids/metabolism/pharmacology ; Hibernation/genetics/physiology ; Larva/growth & development ; Pheromones/metabolism/pharmacology ; Population Density ; Quantitative Trait Loci/genetics ; Receptors, Pheromone/*genetics/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2012-07-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chklovskii, Dmitri B -- Bargmann, Cornelia I -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 27;337(6093):416-7. doi: 10.1126/science.1225853.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, VA 20147, USA. chklovskiid@janelia.hhmi.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22837511" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Caenorhabditis elegans/*physiology/*ultrastructure ; Male ; Nerve Net/*physiology/*ultrastructure ; Neurons/*physiology ; *Sexual Behavior, Animal ; Synapses/*physiology
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2016-01-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chalasani, Sreekanth H -- Chronis, Nikos -- Tsunozaki, Makoto -- Gray, Jesse M -- Ramot, Daniel -- Goodman, Miriam B -- Bargmann, Cornelia I -- England -- Nature. 2016 May 5;533(7601):130. doi: 10.1038/nature16515. Epub 2016 Jan 20.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26789243" target="_blank"〉PubMed〈/a〉
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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