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<pubDate>Thu, 21 Aug 2008 15:28:52 BST</pubDate>


	<title>CiteULike: awooga's Jones</title>
	<description>CiteULike: awooga's Jones</description>


	<link>http://www.citeulike.org/user/awooga/author/Jones</link>
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<item rdf:about="http://www.citeulike.org/user/awooga/article/945537">
    <title>The plant immune system</title>
    <link>http://www.citeulike.org/user/awooga/article/945537</link>
    <description>&lt;i&gt;Nature, Vol. 444, No. 7117., pp. 323-329.&lt;/i&gt;</description>
    <dc:title>The plant immune system</dc:title>

    <dc:creator>Jonathan Jones</dc:creator>
    <dc:creator>Jeffery Dangl</dc:creator>
    <dc:identifier>doi:10.1038/nature05286</dc:identifier>
    <dc:source>Nature, Vol. 444, No. 7117., pp. 323-329.</dc:source>
    <dc:date>2006-11-16T03:45:43-00:00</dc:date>
    <prism:publicationName>Nature</prism:publicationName>
    <prism:issn>0028-0836</prism:issn>
    <prism:volume>444</prism:volume>
    <prism:number>7117</prism:number>
    <prism:startingPage>323</prism:startingPage>
    <prism:endingPage>329</prism:endingPage>
    <prism:publisher>Nature Publishing Group</prism:publisher>
    <prism:category>immunology</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/awooga/article/2523192">
    <title>Unique Properties of Mesoprefrontal Neurons within a Dual Mesocorticolimbic Dopamine System</title>
    <link>http://www.citeulike.org/user/awooga/article/2523192</link>
    <description>&lt;i&gt;Neuron, Vol. 57, No. 5. (13 March 2008), pp. 760-773.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Summary The mesocorticolimbic dopamine system is essential for cognitive and emotive brain functions and is thus an important target in major brain diseases like schizophrenia, drug addiction, and attention deficit hyperactivity disorder. However, the cellular basis for the diversity in behavioral functions and associated dopamine-release pattern within the mesocorticolimbic system has remained unclear. Here, we report the identification of a type of dopaminergic neuron within the mesocorticolimbic dopamine system with unconventional fast-firing properties and small DAT/TH mRNA expression ratios that selectively projects to prefrontal cortex and nucleus accumbens core and medial shell as well as to basolateral amygdala. In contrast, well-described conventional slow-firing dopamine midbrain neurons only project to the lateral shell of the nucleus accumbens and the dorsolateral striatum. Among this dual dopamine midbrain system defined in this study by converging anatomical, electrophysiological, and molecular properties, mesoprefrontal dopaminergic neurons are unique, as only they do not possess functional somatodendritic Girk2-coupled dopamine D2 autoreceptors.</description>
    <dc:title>Unique Properties of Mesoprefrontal Neurons within a Dual Mesocorticolimbic Dopamine System</dc:title>

    <dc:creator>Stephan Lammel</dc:creator>
    <dc:creator>Andrea Hetzel</dc:creator>
    <dc:creator>Olga Hackel</dc:creator>
    <dc:creator>Ian Jones</dc:creator>
    <dc:creator>Birgit Liss</dc:creator>
    <dc:creator>Jochen Roeper</dc:creator>
    <dc:identifier>doi:10.1016/j.neuron.2008.01.022</dc:identifier>
    <dc:source>Neuron, Vol. 57, No. 5. (13 March 2008), pp. 760-773.</dc:source>
    <dc:date>2008-03-13T00:38:04-00:00</dc:date>
    <prism:publicationYear>2008</prism:publicationYear>
    <prism:publicationName>Neuron</prism:publicationName>
    <prism:volume>57</prism:volume>
    <prism:number>5</prism:number>
    <prism:startingPage>760</prism:startingPage>
    <prism:endingPage>773</prism:endingPage>
    <prism:category>autoreceptors</prism:category>
    <prism:category>cortex</prism:category>
    <prism:category>d2-receptor</prism:category>
    <prism:category>dopamine</prism:category>
    <prism:category>substantia-nigra</prism:category>
    <prism:category>vta</prism:category>
</item>



<item rdf:about="http://www.citeulike.org/user/awooga/article/1141837">
    <title>Amphetamine blocks long-term synaptic depression in the ventral tegmental area.</title>
    <link>http://www.citeulike.org/user/awooga/article/1141837</link>
    <description>&lt;i&gt;J Neurosci, Vol. 20, No. 15. (1 August 2000), pp. 5575-5580.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;The mesolimbic dopamine system is essential for reward-seeking behavior, and drugs of abuse are thought to usurp the normal functioning of this pathway. A growing body of evidence suggests that glutamatergic synapses on dopamine neurons in the ventral tegmental area (VTA) are modified during exposure to addictive drugs, producing sensitization, a progressive augmentation in the rewarding properties of psychostimulant drugs with repeated exposure. We have tested the hypothesis that psychostimulant exposure interferes with the synaptic plasticity of glutamatergic inputs to the VTA. We find that excitatory synapses onto VTA dopamine neurons exhibit long-term depression (LTD) in response to low-frequency stimulation and modest depolarization. LTD in the VTA is NMDA receptor-independent but is dependent on intracellular Ca(2+) and can be induced by driving Ca(2+) into the dopamine neuron. Brief exposure to amphetamine entirely blocks LTD at glutamatergic synapses in the VTA, by releasing endogenous dopamine that acts at D2 dopamine receptors. The block of LTD is selective, because amphetamine has no effect on hippocampal LTD. The LTD we have discovered in the VTA is likely to be an important component of excitatory control of the reward pathway; amphetamine will inhibit LTD, removing this normal brake on the glutamatergic drive to dopamine neurons. This effect of amphetamine represents an important mechanism by which normal function of the brain reward system may be impaired during substance abuse.</description>
    <dc:title>Amphetamine blocks long-term synaptic depression in the ventral tegmental area.</dc:title>

    <dc:creator>S Jones</dc:creator>
    <dc:creator>JL Kornblum</dc:creator>
    <dc:creator>JA Kauer</dc:creator>
    <dc:source>J Neurosci, Vol. 20, No. 15. (1 August 2000), pp. 5575-5580.</dc:source>
    <dc:date>2007-03-05T14:49:27-00:00</dc:date>
    <prism:publicationYear>2000</prism:publicationYear>
    <prism:publicationName>J Neurosci</prism:publicationName>
    <prism:issn>0270-6474</prism:issn>
    <prism:volume>20</prism:volume>
    <prism:number>15</prism:number>
    <prism:startingPage>5575</prism:startingPage>
    <prism:endingPage>5580</prism:endingPage>
    <prism:category>no-tag</prism:category>
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