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<pubDate>Thu, 24 Jul 2008 19:35:50 BST</pubDate>


	<title>CiteULike: brembs black</title>
	<description>CiteULike: brembs black</description>


	<link>http://www.citeulike.org/user/brembs/tag/black</link>
	<dc:publisher>CiteULike.org</dc:publisher>
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        <rdf:li rdf:resource="http://www.citeulike.org/user/brembs/article/877190"/>
        <rdf:li rdf:resource="http://www.citeulike.org/user/brembs/article/877186"/>

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<item rdf:about="http://www.citeulike.org/user/brembs/article/877190">
    <title>Drosophila as a new model organism for the neurobiology of aggression?</title>
    <link>http://www.citeulike.org/user/brembs/article/877190</link>
    <description>&lt;i&gt;J Exp Biol, Vol. 205, No. Pt 9. (May 2002), pp. 1233-1240.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;We report here the effects of several neurobiological determinants on aggressive behaviour in the fruitfly Drosophila melanogaster. This study combines behavioural, transgenic, genetic and pharmacological techniques that are well established in the fruitfly, in the novel context of the neurobiology of aggression. We find that octopamine, dopamine and a region in the Drosophila brain called the mushroom bodies, all profoundly influence the expression of aggressive behaviour. Serotonin had no effect. We conclude that Drosophila, with its advanced set of molecular tools and its behavioural richness, has the potential to develop into a new model organism for the study of the neurobiology of aggression.</description>
    <dc:title>Drosophila as a new model organism for the neurobiology of aggression?</dc:title>

    <dc:creator>A Baier</dc:creator>
    <dc:creator>B Wittek</dc:creator>
    <dc:creator>B Brembs</dc:creator>
    <dc:source>J Exp Biol, Vol. 205, No. Pt 9. (May 2002), pp. 1233-1240.</dc:source>
    <dc:date>2006-09-29T06:48:43-00:00</dc:date>
    <prism:publicationYear>2002</prism:publicationYear>
    <prism:publicationName>J Exp Biol</prism:publicationName>
    <prism:issn>0022-0949</prism:issn>
    <prism:volume>205</prism:volume>
    <prism:number>Pt 9</prism:number>
    <prism:startingPage>1233</prism:startingPage>
    <prism:endingPage>1240</prism:endingPage>
    <prism:category>aggression</prism:category>
    <prism:category>behavior</prism:category>
    <prism:category>black</prism:category>
    <prism:category>drosophila</prism:category>
    <prism:category>gene</prism:category>
    <prism:category>genetics</prism:category>
    <prism:category>neurobiology</prism:category>
    <prism:category>neuroscience</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/brembs/article/877186">
    <title>The Drosophila black enigma: the molecular and behavioural characterization of the black1 mutant allele.</title>
    <link>http://www.citeulike.org/user/brembs/article/877186</link>
    <description>&lt;i&gt;Gene, Vol. 351 (23 May 2005), pp. 131-142.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The cuticular melanization phenotype of black flies is rescued by beta-alanine, but beta-alanine production, by aspartate decarboxylation, was reported to be normal in assays of black mutants, and although black/Dgad2 is expressed in the lamina, the first optic ganglion, no electroretinogram (ERG) or other visual defect has been demonstrated in black flies. The purpose of this study was to investigate the black gene, and protein, in black(1) mutants of Drosophila melanogaster in order to resolve the apparent paradox of the black phenotype. Using black(1) mutant flies we show that (1) aspartate decarboxylase activity is significantly reduced in adults and at puparium formation, consistent with defects in cuticular and non-cuticular processes, (2) that the black(1) mutation is a frameshift, and black(1) flies are nulls for the black/DGAD2 protein, and (3) that behavioural experiments using Buridan's paradigm, demonstrate that black responds abnormally to visual cues. No ERG, or target recognition defects can be demonstrated suggesting a problem with higher order visual functions in black mutants.</description>
    <dc:title>The Drosophila black enigma: the molecular and behavioural characterization of the black1 mutant allele.</dc:title>

    <dc:creator>AM Phillips</dc:creator>
    <dc:creator>R Smart</dc:creator>
    <dc:creator>R Strauss</dc:creator>
    <dc:creator>B Brembs</dc:creator>
    <dc:creator>LE Kelly</dc:creator>
    <dc:identifier>doi:10.1016/j.gene.2005.03.013</dc:identifier>
    <dc:source>Gene, Vol. 351 (23 May 2005), pp. 131-142.</dc:source>
    <dc:date>2006-09-29T06:47:26-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Gene</prism:publicationName>
    <prism:issn>0378-1119</prism:issn>
    <prism:volume>351</prism:volume>
    <prism:startingPage>131</prism:startingPage>
    <prism:endingPage>142</prism:endingPage>
    <prism:category>behavior</prism:category>
    <prism:category>black</prism:category>
    <prism:category>drosophila</prism:category>
    <prism:category>gene</prism:category>
    <prism:category>genetics</prism:category>
    <prism:category>neurobiology</prism:category>
    <prism:category>neuroscience</prism:category>
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