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<title>Hippocampal and perirhinal functions in recognition memory</title>
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<description>I would like to correct a statement that was made by Squireet al. in a recent Review of recognition memory. On page 879, the Review states that 'In one study in monkeys72, 34% of hippocampal cells responded differently </description>
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<p>
<b>Hippocampal and perirhinal functions in recognition memory</b>
</p>
<p>Nature Reviews Neuroscience 9, 405 (2008). <a href="http://dx.doi.org/10.1038/nrn2154-c1">doi:10.1038/nrn2154-c1</a>
</p>
<p>Author: Malcolm W. Brown</p>
<p>I would like to correct a statement that was made by Squireet al. in a recent Review of recognition memory. On page 879, the Review states that 'In one study in monkeys72, 34% of hippocampal cells responded differently </p>
]]></content:encoded>
<dc:title>Hippocampal and perirhinal functions in recognition memory</dc:title>
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<dc:source>Nature Reviews Neuroscience 9, 405 (2008)</dc:source>
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<description>Brown objects to a statement in our review that, in his study with monkeys, 34% of hippocampal cells responded differently depending on whether the stimulus was familiar or novel. If familiarity and novelty were defined as Brown defines them, then our statement </description>
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<p>
<b>Review authors' response</b>
</p>
<p>Nature Reviews Neuroscience 9, 405 (2008). <a href="http://dx.doi.org/10.1038/nrn2154-c2">doi:10.1038/nrn2154-c2</a>
</p>
<p>Authors: Larry R. Squire, John T. Wixted
&amp; Robert E. Clark</p>
<p>Brown objects to a statement in our review that, in his study with monkeys, 34% of hippocampal cells responded differently depending on whether the stimulus was familiar or novel. If familiarity and novelty were defined as Brown defines them, then our statement </p>
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<dc:title>Review authors' response</dc:title>
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<title>Metaplasticity: tuning synapses and networks for plasticity</title>
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<description>Synaptic plasticity is a key component of the learning machinery in the brain. It is vital that such plasticity be tightly regulated so that it occurs to the proper extent at the proper time. Activity-dependent mechanisms that have been collectively termed metaplasticity have evolved to </description>
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<p>
<b>Metaplasticity: tuning synapses and networks for plasticity</b>
</p>
<p>Nature Reviews Neuroscience 9, 387 (2008). <a href="http://dx.doi.org/10.1038/nrn2356">doi:10.1038/nrn2356</a>
</p>
<p>Author: Wickliffe C. Abraham</p>
<p>Synaptic plasticity is a key component of the learning machinery in the brain. It is vital that such plasticity be tightly regulated so that it occurs to the proper extent at the proper time. Activity-dependent mechanisms that have been collectively termed metaplasticity have evolved to </p>
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<dc:title>Metaplasticity: tuning synapses and networks for plasticity</dc:title>
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<title>GABAA receptor trafficking and its role in the dynamic modulation of neuronal inhibition</title>
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<description>GABA (&#947;-aminobutyric acid) type A receptors (GABAARs) mediate most fast synaptic inhibition in the mammalian brain, controlling activity at both the network and the cellular levels. The diverse functions of GABA in the CNS are matched not just by the heterogeneity of GABA</description>
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<p>
<b>GABAA receptor trafficking and its role in the dynamic modulation of neuronal inhibition</b>
</p>
<p>Nature Reviews Neuroscience 9, 331 (2008). <a href="http://dx.doi.org/10.1038/nrn2370">doi:10.1038/nrn2370</a>
</p>
<p>Authors: Tija C. Jacob, Stephen J. Moss
&amp; Rachel Jurd</p>
<p>GABA (&#947;-aminobutyric acid) type A receptors (GABAARs) mediate most fast synaptic inhibition in the mammalian brain, controlling activity at both the network and the cellular levels. The diverse functions of GABA in the CNS are matched not just by the heterogeneity of GABA</p>
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<dc:title>GABAA receptor trafficking and its role in the dynamic modulation of neuronal inhibition</dc:title>
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<title>Plasticity of intrinsic neuronal properties in CNS disorders</title>
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<description>The input&#8211;output relationship of neuronal networks depends both on their synaptic connectivity and on the intrinsic properties of their neuronal elements. In addition to altered synaptic properties, profound changes in intrinsic neuronal properties are observed in many CNS disorders. These changes reflect alterations in the </description>
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<p>
<b>Plasticity of intrinsic neuronal properties in CNS disorders</b>
</p>
<p>Nature Reviews Neuroscience 9, 357 (2008). <a href="http://dx.doi.org/10.1038/nrn2371">doi:10.1038/nrn2371</a>
</p>
<p>Authors: Heinz Beck
&amp; Yoel Yaari</p>
<p>The input&#8211;output relationship of neuronal networks depends both on their synaptic connectivity and on the intrinsic properties of their neuronal elements. In addition to altered synaptic properties, profound changes in intrinsic neuronal properties are observed in many CNS disorders. These changes reflect alterations in the </p>
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<title>General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal</title>
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<description>The mechanisms through which general anaesthetics, an extremely diverse group of drugs, cause reversible loss of consciousness have been a long-standing mystery. Gradually, a relatively small number of important molecular targets have emerged, and how these drugs act at the molecular level is becoming clearer. </description>
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<p>
<b>General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal</b>
</p>
<p>Nature Reviews Neuroscience 9, 370 (2008). <a href="http://dx.doi.org/10.1038/nrn2372">doi:10.1038/nrn2372</a>
</p>
<p>Author: Nicholas P. Franks</p>
<p>The mechanisms through which general anaesthetics, an extremely diverse group of drugs, cause reversible loss of consciousness have been a long-standing mystery. Gradually, a relatively small number of important molecular targets have emerged, and how these drugs act at the molecular level is becoming clearer. </p>
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<dc:title>General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal</dc:title>
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<dc:source>Nature Reviews Neuroscience 9, 370 (2008)</dc:source>
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<title>Actin in action: the interplay between the actin cytoskeleton and synaptic efficacy</title>
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<description>Synapse regulation exploits the capacity of actin to function as a stable structural component or as a dynamic filament. Beyond its well-appreciated role in eliciting visible morphological changes at the synapse, the emerging picture points to an active contribution of actin to the modulation of </description>
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<p>
<b>Actin in action: the interplay between the actin cytoskeleton and synaptic efficacy</b>
</p>
<p>Nature Reviews Neuroscience 9, 344 (2008). <a href="http://dx.doi.org/10.1038/nrn2373">doi:10.1038/nrn2373</a>
</p>
<p>Authors: Lorenzo A. Cingolani
&amp; Yukiko Goda</p>
<p>Synapse regulation exploits the capacity of actin to function as a stable structural component or as a dynamic filament. Beyond its well-appreciated role in eliciting visible morphological changes at the synapse, the emerging picture points to an active contribution of actin to the modulation of </p>
]]></content:encoded>
<dc:title>Actin in action: the interplay between the actin cytoskeleton and synaptic efficacy</dc:title>
<dc:creator>Lorenzo A. Cingolani</dc:creator>
<dc:creator>Yukiko Goda</dc:creator>
<dc:identifier>doi:10.1038/nrn2373</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 344 (2008)</dc:source>
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<title>Glia: Space invaders</title>
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<description>Our understanding of the roles of glia in the nervous system has changed drastically in a relatively short time. Astrocytes are now recognized to be much more than 'space-fillers', and it has been shown that cortical astrocyte processes are organized according to strict rules. New </description>
<content:encoded><![CDATA[

<p>
<b>Glia: Space invaders</b>
</p>
<p>Nature Reviews Neuroscience 9, 328 (2008). <a href="http://dx.doi.org/10.1038/nrn2375">doi:10.1038/nrn2375</a>
</p>
<p>Author: Katherine Whalley</p>
<p>Our understanding of the roles of glia in the nervous system has changed drastically in a relatively short time. Astrocytes are now recognized to be much more than 'space-fillers', and it has been shown that cortical astrocyte processes are organized according to strict rules. New </p>
]]></content:encoded>
<dc:title>Glia: Space invaders</dc:title>
<dc:creator>Katherine Whalley</dc:creator>
<dc:identifier>doi:10.1038/nrn2375</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 328 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
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<title>Synaptic plasticity: A depressing TRP</title>
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<description>The transient receptor potential (TRP) family of ion channels has become one of the hottest areas of research; however, little is known about these channels' function in the brain. Kauer and colleagues now reveal that one family member, TRPV1, has a role in a </description>
<content:encoded><![CDATA[

<p>
<b>Synaptic plasticity: A depressing TRP</b>
</p>
<p>Nature Reviews Neuroscience 9, 324 (2008). <a href="http://dx.doi.org/10.1038/nrn2376">doi:10.1038/nrn2376</a>
</p>
<p>Author: Katherine Whalley</p>
<p>The transient receptor potential (TRP) family of ion channels has become one of the hottest areas of research; however, little is known about these channels' function in the brain. Kauer and colleagues now reveal that one family member, TRPV1, has a role in a </p>
]]></content:encoded>
<dc:title>Synaptic plasticity: A depressing TRP</dc:title>
<dc:creator>Katherine Whalley</dc:creator>
<dc:identifier>doi:10.1038/nrn2376</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 324 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
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<title>Multisensory integration: current issues from the perspective of the single neuron</title>
<link>http://dx.doi.org/10.1038/nrn2377</link>
<description>Nature Reviews Neuroscience9, 255&#8211;266 (2008)In Box 2, part a of the above article, the traces representing stimulus onset were incorrectly aligned with the rasters and histograms representing the neuron's responses. The corrected figure is shown below.</description>
<content:encoded><![CDATA[

<p>
<b>Multisensory integration: current issues from the perspective of the single neuron</b>
</p>
<p>Nature Reviews Neuroscience 9, 406 (2008). <a href="http://dx.doi.org/10.1038/nrn2377">doi:10.1038/nrn2377</a>
</p>
<p>Author: Barry E. Stein
&amp; Terrence R. Stanford</p>
<p>Nature Reviews Neuroscience9, 255&#8211;266 (2008)In Box 2, part a of the above article, the traces representing stimulus onset were incorrectly aligned with the rasters and histograms representing the neuron's responses. The corrected figure is shown below.</p>
]]></content:encoded>
<dc:title>Multisensory integration: current issues from the perspective of the single neuron</dc:title>
<dc:creator>Barry E. Stein</dc:creator>
<dc:creator>Terrence R. Stanford</dc:creator>
<dc:identifier>doi:10.1038/nrn2377</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 406 (2008)</dc:source>
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<title>Cell fate: The path to neurogenesis</title>
<link>http://dx.doi.org/10.1038/nrn2378</link>
<description>Neural progenitor cells (NPCs) in the mammalian brain are multipotent: they can differentiate into neurons, astrocytes or oligodendrocytes during development and in healthy adults. However, the factors that influence NPC differentiation remain poorly characterized. A new study shows that, in mice, the cellular redox state </description>
<content:encoded><![CDATA[

<p>
<b>Cell fate: The path to neurogenesis</b>
</p>
<p>Nature Reviews Neuroscience 9, 329 (2008). <a href="http://dx.doi.org/10.1038/nrn2378">doi:10.1038/nrn2378</a>
</p>
<p>Author: Craig Nicholson</p>
<p>Neural progenitor cells (NPCs) in the mammalian brain are multipotent: they can differentiate into neurons, astrocytes or oligodendrocytes during development and in healthy adults. However, the factors that influence NPC differentiation remain poorly characterized. A new study shows that, in mice, the cellular redox state </p>
]]></content:encoded>
<dc:title>Cell fate: The path to neurogenesis</dc:title>
<dc:creator>Craig Nicholson</dc:creator>
<dc:identifier>doi:10.1038/nrn2378</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 329 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>329</prism:startingPage>
<prism:endingPage>329</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2380">
<title>Neurogenetics: Unusual suspects</title>
<link>http://dx.doi.org/10.1038/nrn2380</link>
<description>That genetics plays a part in schizophrenia has been established for some time, yet it is still unknown how the various gene mutations that have been associated with schizophrenia contribute to the disorder. The idea that multiple common mutations, each of which slightly increases the </description>
<content:encoded><![CDATA[

<p>
<b>Neurogenetics: Unusual suspects</b>
</p>
<p>Nature Reviews Neuroscience 9, 326 (2008). <a href="http://dx.doi.org/10.1038/nrn2380">doi:10.1038/nrn2380</a>
</p>
<p>Author: Katherine Whalley</p>
<p>That genetics plays a part in schizophrenia has been established for some time, yet it is still unknown how the various gene mutations that have been associated with schizophrenia contribute to the disorder. The idea that multiple common mutations, each of which slightly increases the </p>
]]></content:encoded>
<dc:title>Neurogenetics: Unusual suspects</dc:title>
<dc:creator>Katherine Whalley</dc:creator>
<dc:identifier>doi:10.1038/nrn2380</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 326 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>326</prism:startingPage>
<prism:endingPage>327</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2381">
<title>Neuroanatomy: A split (mid)brain for dopamine</title>
<link>http://dx.doi.org/10.1038/nrn2381</link>
<description>Dopamine is a versatile neurotransmitter that has a role in movement and many aspects of cognition. Lammel et al. have now characterized two types of neurons in the mesocorticolimbic dopamine system that are not only anatomically segregated, with non-overlapping axonal target regions, but that </description>
<content:encoded><![CDATA[

<p>
<b>Neuroanatomy: A split (mid)brain for dopamine</b>
</p>
<p>Nature Reviews Neuroscience 9, 326 (2008). <a href="http://dx.doi.org/10.1038/nrn2381">doi:10.1038/nrn2381</a>
</p>
<p>Author: Leonie Welberg</p>
<p>Dopamine is a versatile neurotransmitter that has a role in movement and many aspects of cognition. Lammel et al. have now characterized two types of neurons in the mesocorticolimbic dopamine system that are not only anatomically segregated, with non-overlapping axonal target regions, but that </p>
]]></content:encoded>
<dc:title>Neuroanatomy: A split (mid)brain for dopamine</dc:title>
<dc:creator>Leonie Welberg</dc:creator>
<dc:identifier>doi:10.1038/nrn2381</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 326 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
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<prism:endingPage>326</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2382">
<title>Molecular neuroscience: Stress hormones Trk neurons into survival</title>
<link>http://dx.doi.org/10.1038/nrn2382</link>
<description>Glucocorticoids have a bad reputation. However, although these stress hormones can be neurotoxic in high levels, they are also required for neuronal survival, and they promote neuronal growth and differentiation and support synaptic plasticity in the hippocampus. Chao and colleagues now show that, in rats, </description>
<content:encoded><![CDATA[

<p>
<b>Molecular neuroscience: Stress hormones Trk neurons into survival</b>
</p>
<p>Nature Reviews Neuroscience 9, 328 (2008). <a href="http://dx.doi.org/10.1038/nrn2382">doi:10.1038/nrn2382</a>
</p>
<p>Author: Leonie Welberg</p>
<p>Glucocorticoids have a bad reputation. However, although these stress hormones can be neurotoxic in high levels, they are also required for neuronal survival, and they promote neuronal growth and differentiation and support synaptic plasticity in the hippocampus. Chao and colleagues now show that, in rats, </p>
]]></content:encoded>
<dc:title>Molecular neuroscience: Stress hormones Trk neurons into survival</dc:title>
<dc:creator>Leonie Welberg</dc:creator>
<dc:identifier>doi:10.1038/nrn2382</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 328 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>328</prism:startingPage>
<prism:endingPage>329</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2383">
<title>Microglia: Giving out dangerous signals</title>
<link>http://dx.doi.org/10.1038/nrn2383</link>
<description>Microglia mediate potent innate immune responses to both infectious and traumatic challenges. However, they are not always neuroprotective, as upon activation they can accelerate neurodegeneration. The precise mechanism by which this happens is unclear. Now, Lehnardt et al. report that release of the heat-shock </description>
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<p>
<b>Microglia: Giving out dangerous signals</b>
</p>
<p>Nature Reviews Neuroscience 9, 326 (2008). <a href="http://dx.doi.org/10.1038/nrn2383">doi:10.1038/nrn2383</a>
</p>
<p>Author: Monica Hoyos Flight</p>
<p>Microglia mediate potent innate immune responses to both infectious and traumatic challenges. However, they are not always neuroprotective, as upon activation they can accelerate neurodegeneration. The precise mechanism by which this happens is unclear. Now, Lehnardt et al. report that release of the heat-shock </p>
]]></content:encoded>
<dc:title>Microglia: Giving out dangerous signals</dc:title>
<dc:creator>Monica Hoyos Flight</dc:creator>
<dc:identifier>doi:10.1038/nrn2383</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 326 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>326</prism:startingPage>
<prism:endingPage>327</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2384">
<title>Botoxic transportation</title>
<link>http://dx.doi.org/10.1038/nrn2384</link>
<description>It is widely known that Botox exerts its wrinkle-decreasing effects through its toxicity for nerve cells: it was considered to be safe for clinical use because those effects were thought to be localized to the site of its injection. There is growing concern, however, that </description>
<content:encoded><![CDATA[

<p>
<b>Botoxic transportation</b>
</p>
<p>Nature Reviews Neuroscience 9, 325 (2008). <a href="http://dx.doi.org/10.1038/nrn2384">doi:10.1038/nrn2384</a>
</p>
<p>Author: Craig Nicholson</p>
<p>It is widely known that Botox exerts its wrinkle-decreasing effects through its toxicity for nerve cells: it was considered to be safe for clinical use because those effects were thought to be localized to the site of its injection. There is growing concern, however, that </p>
]]></content:encoded>
<dc:title>Botoxic transportation</dc:title>
<dc:creator>Craig Nicholson</dc:creator>
<dc:identifier>doi:10.1038/nrn2384</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 325 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>325</prism:startingPage>
<prism:endingPage>325</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2385">
<title>From the editors</title>
<link>http://dx.doi.org/10.1038/nrn2385</link>
<description>Neuronal excitability is to a large extent controlled by the type and number of receptors and ion channels present on the cell surface. On page 331 of this issue, Moss and colleagues authoritatively review the regulation of the composition of GABAA receptors </description>
<content:encoded><![CDATA[

<p>
<b>From the editors</b>
</p>
<p>Nature Reviews Neuroscience 9, 321 (2008). <a href="http://dx.doi.org/10.1038/nrn2385">doi:10.1038/nrn2385</a>
</p>
<p>Neuronal excitability is to a large extent controlled by the type and number of receptors and ion channels present on the cell surface. On page 331 of this issue, Moss and colleagues authoritatively review the regulation of the composition of GABAA receptors </p>
]]></content:encoded>
<dc:title>From the editors</dc:title>
<dc:identifier>doi:10.1038/nrn2385</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 321 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>From The Editors</prism:section>
<prism:startingPage>321</prism:startingPage>
<prism:endingPage>321</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2386">
<title>Choices in neuroscience careers</title>
<link>http://dx.doi.org/10.1038/nrn2386</link>
<description>How do I choose a mentor? How do I decide what field of neuroscience to work in? Should I consider doing research in industry? Most students and postdoctoral researchers aiming for a successful career in neuroscience ask themselves these questions. In this article, Nature Reviews </description>
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<p>
<b>Choices in neuroscience careers</b>
</p>
<p>Nature Reviews Neuroscience 9, 401 (2008). <a href="http://dx.doi.org/10.1038/nrn2386">doi:10.1038/nrn2386</a>
</p>
<p>Author: Tamas Bartfai, Tom Insel, Gord Fishell
&amp; Nancy Rothwell</p>
<p>How do I choose a mentor? How do I decide what field of neuroscience to work in? Should I consider doing research in industry? Most students and postdoctoral researchers aiming for a successful career in neuroscience ask themselves these questions. In this article, Nature Reviews </p>
]]></content:encoded>
<dc:title>Choices in neuroscience careers</dc:title>
<dc:creator>Tamas Bartfai</dc:creator>
<dc:creator>Tom Insel</dc:creator>
<dc:creator>Gord Fishell</dc:creator>
<dc:creator>Nancy Rothwell</dc:creator>
<dc:identifier>doi:10.1038/nrn2386</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 401 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Perspective</prism:section>
<prism:startingPage>401</prism:startingPage>
<prism:endingPage>405</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2387">
<title>Neuroprotection: Staying active = staying alive</title>
<link>http://dx.doi.org/10.1038/nrn2387</link>
<description>Overactivation of NMDA (N-methyl-D-aspartate) receptors (NMDARs) can lead to excitotoxicity, possibly through the production of free radicals. However, Hardingham and colleagues now show that NMDAR activity in synapses, but not at extra-synaptic sites, in fact has neuroprotective effects through stimulation of </description>
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<p>
<b>Neuroprotection: Staying active = staying alive</b>
</p>
<p>Nature Reviews Neuroscience 9, 325 (2008). <a href="http://dx.doi.org/10.1038/nrn2387">doi:10.1038/nrn2387</a>
</p>
<p>Author: Leonie Welberg</p>
<p>Overactivation of NMDA (N-methyl-D-aspartate) receptors (NMDARs) can lead to excitotoxicity, possibly through the production of free radicals. However, Hardingham and colleagues now show that NMDAR activity in synapses, but not at extra-synaptic sites, in fact has neuroprotective effects through stimulation of </p>
]]></content:encoded>
<dc:title>Neuroprotection: Staying active = staying alive</dc:title>
<dc:creator>Leonie Welberg</dc:creator>
<dc:identifier>doi:10.1038/nrn2387</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 325 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>325</prism:startingPage>
<prism:endingPage>325</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2388">
<title>In brief</title>
<link>http://dx.doi.org/10.1038/nrn2388</link>
<description>NeurogeneticsNPY</description>
<content:encoded><![CDATA[

<p>
<b>In brief</b>
</p>
<p>Nature Reviews Neuroscience 9, 324 (2008). <a href="http://dx.doi.org/10.1038/nrn2388">doi:10.1038/nrn2388</a>
</p>
<p>NeurogeneticsNPY</p>
]]></content:encoded>
<dc:title>In brief</dc:title>
<dc:identifier>doi:10.1038/nrn2388</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 324 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>324</prism:startingPage>
<prism:endingPage>324</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2389">
<title>In brief</title>
<link>http://dx.doi.org/10.1038/nrn2389</link>
<description>NeuroimagingThe maturing architecture of the brain's default networkFair, D. A.et al. Proc. Natl Acad. Sci. USA105, 4028&#8211;4032 (2008)The 'default network' consists of brain areas in which activity decreases during goal-oriented tasks. The </description>
<content:encoded><![CDATA[

<p>
<b>In brief</b>
</p>
<p>Nature Reviews Neuroscience 9, 327 (2008). <a href="http://dx.doi.org/10.1038/nrn2389">doi:10.1038/nrn2389</a>
</p>
<p>NeuroimagingThe maturing architecture of the brain's default networkFair, D. A.et al. Proc. Natl Acad. Sci. USA105, 4028&#8211;4032 (2008)The 'default network' consists of brain areas in which activity decreases during goal-oriented tasks. The </p>
]]></content:encoded>
<dc:title>In brief</dc:title>
<dc:identifier>doi:10.1038/nrn2389</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 327 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>327</prism:startingPage>
<prism:endingPage>327</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrn2390">
<title>Neurodegenerative disease: Understanding and preventing total catastrophe</title>
<link>http://dx.doi.org/10.1038/nrn2390</link>
<description>Polyglutamine diseases are progressive neurodegenerative diseases characterized by the presence of extended CAG repeats in specific genes, such as ataxin 1; these repeats lead to the generation of polyglutamine-expanded (polyQ) proteins. The mechanism by which polyQ proteins cause disease is not known. One study </description>
<content:encoded><![CDATA[

<p>
<b>Neurodegenerative disease: Understanding and preventing total catastrophe</b>
</p>
<p>Nature Reviews Neuroscience 9, 323 (2008). <a href="http://dx.doi.org/10.1038/nrn2390">doi:10.1038/nrn2390</a>
</p>
<p>Author: Claudia Wiedemann</p>
<p>Polyglutamine diseases are progressive neurodegenerative diseases characterized by the presence of extended CAG repeats in specific genes, such as ataxin 1; these repeats lead to the generation of polyglutamine-expanded (polyQ) proteins. The mechanism by which polyQ proteins cause disease is not known. One study </p>
]]></content:encoded>
<dc:title>Neurodegenerative disease: Understanding and preventing total catastrophe</dc:title>
<dc:creator>Claudia Wiedemann</dc:creator>
<dc:identifier>doi:10.1038/nrn2390</dc:identifier>
<dc:source>Nature Reviews Neuroscience 9, 323 (2008)</dc:source>
<prism:publicationName>Nature Reviews Neuroscience</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>323</prism:startingPage>
<prism:endingPage>323</prism:endingPage>
</item>
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