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  • Cell Line  (25)
  • *Biological Evolution  (23)
  • Mice, Inbred C57BL  (17)
  • Population Density  (17)
  • American Association for the Advancement of Science (AAAS)  (81)
  • 2005-2009  (81)
  • 1950-1954
  • 2006  (81)
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  • American Association for the Advancement of Science (AAAS)  (81)
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  • 2005-2009  (81)
  • 1950-1954
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  • 1
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    Phytophthora genome sequences uncover evolutionary origins and mechanisms of pathogenesis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-09-02
    Description: Draft genome sequences have been determined for the soybean pathogen Phytophthora sojae and the sudden oak death pathogen Phytophthora ramorum. Oomycetes such as these Phytophthora species share the kingdom Stramenopila with photosynthetic algae such as diatoms, and the presence of many Phytophthora genes of probable phototroph origin supports a photosynthetic ancestry for the stramenopiles. Comparison of the two species' genomes reveals a rapid expansion and diversification of many protein families associated with plant infection such as hydrolases, ABC transporters, protein toxins, proteinase inhibitors, and, in particular, a superfamily of 700 proteins with similarity to known oomycete avirulence genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tyler, Brett M -- Tripathy, Sucheta -- Zhang, Xuemin -- Dehal, Paramvir -- Jiang, Rays H Y -- Aerts, Andrea -- Arredondo, Felipe D -- Baxter, Laura -- Bensasson, Douda -- Beynon, Jim L -- Chapman, Jarrod -- Damasceno, Cynthia M B -- Dorrance, Anne E -- Dou, Daolong -- Dickerman, Allan W -- Dubchak, Inna L -- Garbelotto, Matteo -- Gijzen, Mark -- Gordon, Stuart G -- Govers, Francine -- Grunwald, Niklaus J -- Huang, Wayne -- Ivors, Kelly L -- Jones, Richard W -- Kamoun, Sophien -- Krampis, Konstantinos -- Lamour, Kurt H -- Lee, Mi-Kyung -- McDonald, W Hayes -- Medina, Monica -- Meijer, Harold J G -- Nordberg, Eric K -- Maclean, Donald J -- Ospina-Giraldo, Manuel D -- Morris, Paul F -- Phuntumart, Vipaporn -- Putnam, Nicholas H -- Rash, Sam -- Rose, Jocelyn K C -- Sakihama, Yasuko -- Salamov, Asaf A -- Savidor, Alon -- Scheuring, Chantel F -- Smith, Brian M -- Sobral, Bruno W S -- Terry, Astrid -- Torto-Alalibo, Trudy A -- Win, Joe -- Xu, Zhanyou -- Zhang, Hongbin -- Grigoriev, Igor V -- Rokhsar, Daniel S -- Boore, Jeffrey L -- BB/C509123/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- New York, N.Y. -- Science. 2006 Sep 1;313(5791):1261-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Virginia Bioinformatics Institute, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061, USA. bmtyler@vt.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16946064" target="_blank"〉PubMed〈/a〉
    Keywords: Algal Proteins/genetics/physiology ; *Biological Evolution ; DNA, Algal/*genetics ; Genes ; *Genome ; Hydrolases/genetics/metabolism ; Photosynthesis/genetics ; Phylogeny ; Physical Chromosome Mapping ; Phytophthora/classification/*genetics/*pathogenicity/physiology ; Plant Diseases/microbiology ; Polymorphism, Single Nucleotide ; Repetitive Sequences, Nucleic Acid ; Sequence Analysis, DNA ; Symbiosis ; Toxins, Biological/genetics
    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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  • 2
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    Netrins promote developmental and therapeutic angiogenesis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-01
    Description: Axonal guidance and vascular patterning share several guidance cues, including proteins in the netrin family. We demonstrate that netrins stimulate proliferation, migration, and tube formation of human endothelial cells in vitro and that this stimulation is independent of known netrin receptors. Suppression of netrin1a messenger RNA in zebrafish inhibits vascular sprouting, implying a proangiogenic role for netrins during vertebrate development. We also show that netrins accelerate neovascularization in an in vivo model of ischemia and that they reverse neuropathy and vasculopathy in a diabetic murine model. We propose that the attractive vascular and neural guidance functions of netrins offer a unique therapeutic potential.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2577078/" 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/PMC2577078/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, Brent D -- Ii, Masaaki -- Park, Kye Won -- Suli, Arminda -- Sorensen, Lise K -- Larrieu-Lahargue, Frederic -- Urness, Lisa D -- Suh, Wonhee -- Asai, Jun -- Kock, Gerhardus A H -- Thorne, Tina -- Silver, Marcy -- Thomas, Kirk R -- Chien, Chi-Bin -- Losordo, Douglas W -- Li, Dean Y -- R01 HL068873/HL/NHLBI NIH HHS/ -- R01 HL077671/HL/NHLBI NIH HHS/ -- R01 HL077671-03/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Aug 4;313(5787):640-4. Epub 2006 Jun 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, UT 84112, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16809490" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inducing Agents ; Animals ; Cell Line ; Cell Movement ; Chemotaxis ; DNA, Complementary ; Diabetic Angiopathies/therapy ; Diabetic Neuropathies/therapy ; Embryo, Nonmammalian ; Endothelial Cells/*physiology ; Endothelium, Vascular/cytology ; Genetic Therapy ; Humans ; Ischemia/drug therapy ; Mice ; Muscle, Skeletal/blood supply ; *Neovascularization, Physiologic ; Nerve Growth Factors/genetics/pharmacology/*physiology ; Neural Conduction ; Receptors, Cell Surface/physiology ; Tumor Suppressor Proteins/genetics/pharmacology/*physiology ; Vascular Endothelial Growth Factor A/therapeutic use ; Zebrafish
    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
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    Planktonic foraminifera of the California Current reflect 20th-century warming (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-01-10
    Description: It is currently unclear whether observed pelagic ecosystem responses to ocean warming, such as a mid-1970s change in the eastern North Pacific, depart from typical ocean variability. We report variations in planktonic foraminifera from varved sediments off southern California spanning the past 1400 years. Increasing abundances of tropical/subtropical species throughout the 20th century reflect a warming trend superimposed on decadal-scale fluctuations. Decreasing abundances of temperate/subpolar species in the late 20th century indicate a deep, penetrative warming not observed in previous centuries. These results imply that 20th-century warming, apparently anthropogenic, has already affected lower trophic levels of the California Current.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Field, David B -- Baumgartner, Timothy R -- Charles, Christopher D -- Ferreira-Bartrina, Vicente -- Ohman, Mark D -- New York, N.Y. -- Science. 2006 Jan 6;311(5757):63-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Scripps Institution of Oceanography, University of California, San Diego, La Jolla, CA 92093, USA. dfield@mbari.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16400144" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; California ; *Climate ; *Ecosystem ; Environment ; *Eukaryota/classification ; *Geologic Sediments ; Greenhouse Effect ; Population Density ; Population Dynamics ; Principal Component Analysis ; Seasons ; Temperature ; Time Factors ; *Zooplankton/classification
    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
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    From disorder to order in marching locusts (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-03
    Description: Recent models from theoretical physics have predicted that mass-migrating animal groups may share group-level properties, irrespective of the type of animals in the group. One key prediction is that as the density of animals in the group increases, a rapid transition occurs from disordered movement of individuals within the group to highly aligned collective motion. Understanding such a transition is crucial to the control of mobile swarming insect pests such as the desert locust. We confirmed the prediction of a rapid transition from disordered to ordered movement and identified a critical density for the onset of coordinated marching in locust nymphs. We also demonstrated a dynamic instability in motion at densities typical of locusts in the field, in which groups can switch direction without external perturbation, potentially facilitating the rapid transfer of directional information.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buhl, J -- Sumpter, D J T -- Couzin, I D -- Hale, J J -- Despland, E -- Miller, E R -- Simpson, S J -- New York, N.Y. -- Science. 2006 Jun 2;312(5778):1402-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK. jbuhl@usyd.edu.au〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16741126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Grasshoppers/*physiology ; *Mass Behavior ; *Models, Biological ; Movement ; Population Density
    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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    Sequencing and analysis of Neanderthal genomic DNA (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-11-18
    Description: Our knowledge of Neanderthals is based on a limited number of remains and artifacts from which we must make inferences about their biology, behavior, and relationship to ourselves. Here, we describe the characterization of these extinct hominids from a new perspective, based on the development of a Neanderthal metagenomic library and its high-throughput sequencing and analysis. Several lines of evidence indicate that the 65,250 base pairs of hominid sequence so far identified in the library are of Neanderthal origin, the strongest being the ascertainment of sequence identities between Neanderthal and chimpanzee at sites where the human genomic sequence is different. These results enabled us to calculate the human-Neanderthal divergence time based on multiple randomly distributed autosomal loci. Our analyses suggest that on average the Neanderthal genomic sequence we obtained and the reference human genome sequence share a most recent common ancestor approximately 706,000 years ago, and that the human and Neanderthal ancestral populations split approximately 370,000 years ago, before the emergence of anatomically modern humans. Our finding that the Neanderthal and human genomes are at least 99.5% identical led us to develop and successfully implement a targeted method for recovering specific ancient DNA sequences from metagenomic libraries. This initial analysis of the Neanderthal genome advances our understanding of the evolutionary relationship of Homo sapiens and Homo neanderthalensis and signifies the dawn of Neanderthal genomics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2583069/" 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/PMC2583069/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Noonan, James P -- Coop, Graham -- Kudaravalli, Sridhar -- Smith, Doug -- Krause, Johannes -- Alessi, Joe -- Chen, Feng -- Platt, Darren -- Paabo, Svante -- Pritchard, Jonathan K -- Rubin, Edward M -- 1-F32-GM074367/GM/NIGMS NIH HHS/ -- HL066681/HL/NHLBI NIH HHS/ -- R01 HG002772/HG/NHGRI NIH HHS/ -- R01 HG002772-01/HG/NHGRI NIH HHS/ -- R01 HG002772-1/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2006 Nov 17;314(5802):1113-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Energy Joint Genome Institute, 2800 Mitchell Drive, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17110569" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Bone and Bones ; Cell Nucleus ; DNA/*genetics/isolation & purification ; DNA, Mitochondrial ; *Fossils ; Gene Pool ; Genome ; Genome, Human ; Genomic Library ; History, Ancient ; Hominidae/*genetics ; Humans ; Male ; Molecular Sequence Data ; Pan troglodytes/genetics ; Polymerase Chain Reaction ; Sequence Alignment ; *Sequence Analysis, DNA/methods ; Time
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
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    Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-10-07
    Description: A common single-nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene, a methionine (Met) substitution for valine (Val) at codon 66 (Val66Met), is associated with alterations in brain anatomy and memory, but its relevance to clinical disorders is unclear. We generated a variant BDNF mouse (BDNF(Met/Met)) that reproduces the phenotypic hallmarks in humans with the variant allele. BDNF(Met) was expressed in brain at normal levels, but its secretion from neurons was defective. When placed in stressful settings, BDNF(Met/Met) mice exhibited increased anxiety-related behaviors that were not normalized by the antidepressant, fluoxetine. A variant BDNF may thus play a key role in genetic predispositions to anxiety and depressive disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1880880/" 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/PMC1880880/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhe-Yu -- Jing, Deqiang -- Bath, Kevin G -- Ieraci, Alessandro -- Khan, Tanvir -- Siao, Chia-Jen -- Herrera, Daniel G -- Toth, Miklos -- Yang, Chingwen -- McEwen, Bruce S -- Hempstead, Barbara L -- Lee, Francis S -- MH060478/MH/NIMH NIH HHS/ -- MH068850/MH/NIMH NIH HHS/ -- NS052819/NS/NINDS NIH HHS/ -- NS30687/NS/NINDS NIH HHS/ -- R01 NS052819/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 Oct 6;314(5796):140-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Weill Medical College of Cornell University, New York, NY 10021, USA. zheyuchen@sdu.edu.cn〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17023662" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Anxiety/drug therapy/*genetics ; Behavior, Animal ; Brain-Derived Neurotrophic Factor/*genetics/*physiology ; Conditioning (Psychology) ; Dendrites/ultrastructure ; Dentate Gyrus/cytology ; Fear ; Fluoxetine/administration & dosage/pharmacology ; Hippocampus/anatomy & histology/metabolism ; Memory ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Motor Activity ; Neurons/cytology/metabolism ; Organ Size ; *Polymorphism, Single Nucleotide ; Rats ; Rats, Sprague-Dawley ; Serotonin Uptake Inhibitors/administration & dosage/pharmacology
    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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  • 7
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    A critical role for the innate immune signaling molecule IRAK-4 in T cell activation (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-01
    Description: IRAK-4 is a protein kinase that is pivotal in mediating signals for innate immune responses. Here, we report that IRAK-4 signaling is also essential for eliciting adaptive immune responses. Thus, in the absence of IRAK-4, in vivo T cell responses were significantly impaired. Upon T cell receptor stimulation, IRAK-4 is recruited to T cell lipid rafts, where it induces downstream signals, including protein kinase C activation through the association with Zap70. This signaling pathway was found to be required for optimal activation of nuclear factor kappaB. Our findings suggest that T cells use this critical regulator of innate immunity for the development of acquired immunity, suggesting that IRAK-4 may be involved in direct signal cross talk between the two systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzuki, Nobutaka -- Suzuki, Shinobu -- Millar, Douglas G -- Unno, Midori -- Hara, Hiromitsu -- Calzascia, Thomas -- Yamasaki, Sho -- Yokosuka, Tadashi -- Chen, Nien-Jung -- Elford, Alisha R -- Suzuki, Jun-Ichiro -- Takeuchi, Arata -- Mirtsos, Christine -- Bouchard, Denis -- Ohashi, Pamela S -- Yeh, Wen-Chen -- Saito, Takashi -- New York, N.Y. -- Science. 2006 Mar 31;311(5769):1927-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Signaling, RIKEN Research Center for Allergy and Immunology, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama City, Kanagawa 230-0045, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16574867" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Activation ; Immunity, Innate ; Interleukin-1 Receptor-Associated Kinases ; Isoenzymes/metabolism ; *Lymphocyte Activation ; Membrane Microdomains/enzymology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; NF-kappa B/metabolism ; Phosphotransferases (Alcohol Group Acceptor)/genetics/*metabolism ; Protein Kinase C/metabolism ; Receptors, Antigen, T-Cell/immunology ; Signal Transduction ; T-Lymphocytes/*immunology ; ZAP-70 Protein-Tyrosine Kinase/metabolism
    Print ISSN: 0036-8075
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  • 8
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    Role of noradrenergic signaling by the nucleus tractus solitarius in mediating opiate reward (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-18
    Description: Norepinephrine (NE) is widely implicated in opiate withdrawal, but much less is known about its role in opiate-induced locomotion and reward. In mice lacking dopamine beta-hydroxylase (DBH), an enzyme critical for NE synthesis, we found that NE was necessary for morphine-induced conditioned place preference (CPP; a measure of reward) and locomotion. These deficits were rescued by systemic NE restoration. Viral restoration of DBH expression in the nucleus tractus solitarius, but not in the locus coeruleus, restored CPP for morphine. Morphine-induced locomotion was partially restored by DBH expression in either brain region. These data suggest that NE signaling by the nucleus tractus solitarius is necessary for morphine reward.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Olson, Valerie G -- Heusner, Carrie L -- Bland, Ross J -- During, Matthew J -- Weinshenker, David -- Palmiter, Richard D -- New York, N.Y. -- Science. 2006 Feb 17;311(5763):1017-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16484499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Conditioning (Psychology) ; Dopamine beta-Hydroxylase/genetics/metabolism ; Droxidopa/pharmacology ; Locomotion/drug effects ; Locus Coeruleus/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Morphine/*pharmacology ; Motor Activity/drug effects ; Norepinephrine/*physiology ; *Reward ; Signal Transduction ; Solitary Nucleus/*physiology ; *Synaptic Transmission
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    CRACM1 is a plasma membrane protein essential for store-operated Ca2+ entry (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-29
    Description: Store-operated Ca2+ entry is mediated by Ca2+ release-activated Ca2+ (CRAC) channels following Ca2+ release from intracellular stores. We performed a genome-wide RNA interference (RNAi) screen in Drosophila cells to identify proteins that inhibit store-operated Ca2+ influx. A secondary patch-clamp screen identified CRACM1 and CRACM2 (CRAC modulators 1 and 2) as modulators of Drosophila CRAC currents. We characterized the human ortholog of CRACM1, a plasma membrane-resident protein encoded by gene FLJ14466. Although overexpression of CRACM1 did not affect CRAC currents, RNAi-mediated knockdown disrupted its activation. CRACM1 could be the CRAC channel itself, a subunit of it, or a component of the CRAC signaling machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vig, M -- Peinelt, C -- Beck, A -- Koomoa, D L -- Rabah, D -- Koblan-Huberson, M -- Kraft, S -- Turner, H -- Fleig, A -- Penner, R -- Kinet, J-P -- 5-R37-GM053950/GM/NIGMS NIH HHS/ -- R01-AI050200/AI/NIAID NIH HHS/ -- R01-GM065360/GM/NIGMS NIH HHS/ -- R01-NS040927/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2006 May 26;312(5777):1220-3. Epub 2006 Apr 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. mvig@bidmc.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16645049" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Cell Line ; Cell Membrane/metabolism ; Drosophila Proteins/*genetics/*metabolism ; Drosophila melanogaster/*metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Ion Transport ; Jurkat Cells ; Membrane Proteins/genetics/*metabolism ; Patch-Clamp Techniques ; RNA Interference ; RNA, Small Interfering ; Reverse Transcriptase Polymerase Chain Reaction
    Print ISSN: 0036-8075
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  • 10
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    Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-14
    Description: Mice experiencing repeated aggression develop a long-lasting aversion to social contact, which can be normalized by chronic, but not acute, administration of antidepressant. Using viral-mediated, mesolimbic dopamine pathway-specific knockdown of brain-derived neurotrophic factor (BDNF), we showed that BDNF is required for the development of this experience-dependent social aversion. Gene profiling in the nucleus accumbens indicates that local knockdown of BDNF obliterates most of the effects of repeated aggression on gene expression within this circuit, with similar effects being produced by chronic treatment with antidepressant. These results establish an essential role for BDNF in mediating long-term neural and behavioral plasticity in response to aversive social experiences.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berton, Olivier -- McClung, Colleen A -- Dileone, Ralph J -- Krishnan, Vaishnav -- Renthal, William -- Russo, Scott J -- Graham, Danielle -- Tsankova, Nadia M -- Bolanos, Carlos A -- Rios, Maribel -- Monteggia, Lisa M -- Self, David W -- Nestler, Eric J -- New York, N.Y. -- Science. 2006 Feb 10;311(5762):864-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Center for Basic Neuroscience, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9070, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16469931" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression ; Animals ; Antidepressive Agents/pharmacology ; Brain-Derived Neurotrophic Factor/genetics/*physiology ; Depression/physiopathology ; Dominance-Subordination ; Dopamine/*physiology ; Fluoxetine/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation/drug effects ; Imipramine/pharmacology ; Limbic System/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/physiology ; Nucleus Accumbens/*physiology ; Oligonucleotide Array Sequence Analysis ; Proto-Oncogene Proteins c-fos/biosynthesis ; *Social Behavior ; Social Isolation ; *Stress, Psychological ; Ventral Tegmental Area/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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