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<title>Nature Neuroscience</title>
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<link>http://www.nature.com/neuro/</link>
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<item rdf:about="http://dx.doi.org/10.1038/nn.2430">
<title>Self-modulation of neocortical pyramidal neurons by endocannabinoids</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/kCZJBJGKTu8/nn.2430</link>
<description>This study finds that excitatory neurons in cortical layer 2/3 can respond to their own firing with persistent hyperpolarization, termed slow self-inhibition or SSI. This process is mediated by endocannabinoids and regulates neuronal excitability.</description>
<content:encoded><![CDATA[

<p>
<b>Self-modulation of neocortical pyramidal neurons by endocannabinoids</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2430">doi:10.1038/nn.2430</a>
</p>
<p>Authors: Silvia Marinelli, Simone Pacioni, Astrid Cannich, Giovanni Marsicano &amp; Alberto Bacci</p>
<p>Control of pyramidal neuron excitability is vital for the functioning of the neocortex. Somatodendritic slow self-inhibition (SSI) allows inhibitory neurons to regulate their own activity, but the existence of similar mechanisms in excitatory cells has not been shown. We found that in rodents endocannabinoids mediated SSI and long-term modulation of inhibitory connections in layer 2/3 pyramidal neurons with a distinct dendritic morphology, suggesting that a glutamatergic network in cortical circuits is self-regulated.</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/kCZJBJGKTu8" height="1" width="1"/>]]></content:encoded>
<dc:title>Self-modulation of neocortical pyramidal neurons by endocannabinoids</dc:title>
<dc:creator>Silvia Marinelli</dc:creator>
<dc:creator>Simone Pacioni</dc:creator>
<dc:creator>Astrid Cannich</dc:creator>
<dc:creator>Giovanni Marsicano</dc:creator>
<dc:creator>Alberto Bacci</dc:creator>
<dc:identifier>doi:10.1038/nn.2430</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-15</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-15</prism:publicationDate>
<prism:doi>10.1038/nn.2430</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2430</prism:url>
<prism:section>Brief Communication</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2430</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2459">
<title>Thrombospondin 1 accelerates synaptogenesis in hippocampal neurons through neuroligin 1</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/uHL62Vvoee4/nn.2459</link>
<description>In cultured rat hippocampal neurons, thrombospondin 1 hastened synapse formation via interaction with neuroligin 1.</description>
<content:encoded><![CDATA[

<p>
<b>Thrombospondin 1 accelerates synaptogenesis in hippocampal neurons through neuroligin 1</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2459">doi:10.1038/nn.2459</a>
</p>
<p>Authors: Junyu Xu, Nan Xiao &amp; Jun Xia</p>
<p>In cultured rat hippocampal neurons, we found that thrombospondin 1 (TSP1) increased the speed of synapse formation in young neurons, but not the final density of synapses in mature neurons. TSP1 interacted with neuroligin 1 (NL1) and application of the NL1 extracellular domain blocked TSP1-induced synaptogenesis. Furthermore, knocking down endogenous NL1 inhibited TSP1's effect. Our results indicate that TSP1 accelerates the speed of synaptogenesis through NL1 in hippocampal neurons.</p>
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<dc:title>Thrombospondin 1 accelerates synaptogenesis in hippocampal neurons through neuroligin 1</dc:title>
<dc:creator>Junyu Xu</dc:creator>
<dc:creator>Nan Xiao</dc:creator>
<dc:creator>Jun Xia</dc:creator>
<dc:identifier>doi:10.1038/nn.2459</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-15</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-15</prism:publicationDate>
<prism:doi>10.1038/nn.2459</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2459</prism:url>
<prism:section>Brief Communication</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2459</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2460">
<title>Dissociable cost and benefit encoding of future rewards by mesolimbic dopamine</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/Y2gZW3fL7DQ/nn.2460</link>
<description>Cue-evoked activity of midbrain dopamine neurons is proposed to encode the magnitude, delay and uncertainty of predicted rewards. Here the authors report that this activity separates costs and benefits, as it does not encode the costs of the action required to obtain predicted rewards.</description>
<content:encoded><![CDATA[

<p>
<b>Dissociable cost and benefit encoding of future rewards by mesolimbic dopamine</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2460">doi:10.1038/nn.2460</a>
</p>
<p>Authors: Jerylin O Gan, Mark E Walton &amp; Paul E M Phillips</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/Y2gZW3fL7DQ" height="1" width="1"/>]]></content:encoded>
<dc:title>Dissociable cost and benefit encoding of future rewards by mesolimbic dopamine</dc:title>
<dc:creator>Jerylin O Gan</dc:creator>
<dc:creator>Mark E Walton</dc:creator>
<dc:creator>Paul E M Phillips</dc:creator>
<dc:identifier>doi:10.1038/nn.2460</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-10</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-10</prism:publicationDate>
<prism:doi>10.1038/nn.2460</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2460</prism:url>
<prism:section>Brief Communication</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2460</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2428">
<title>Experience-dependent compartmentalized dendritic plasticity in rat hippocampal CA1 pyramidal neurons</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/OM3UKfZbM40/nn.2428</link>
<description>Dendritic excitability is a plastic property of neurons. This study shows that exposure to an enriched environment increases propagation of dendritic sodium spikes in a subset of dendritic branches in CA1 pyramidal neurons. This effect is mediated by localized downregulation of A-type potassium channel function.</description>
<content:encoded><![CDATA[

<p>
<b>Experience-dependent compartmentalized dendritic plasticity in rat hippocampal CA1 pyramidal neurons</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2428">doi:10.1038/nn.2428</a>
</p>
<p>Authors: Judit K Makara, Attila Losonczy, Quan Wen &amp; Jeffrey C Magee</p>
<p>The excitability of individual dendritic branches is a plastic property of neurons. We found that experience in an enriched environment increased propagation of dendritic Na+ spikes in a subset of individual dendritic branches in rat hippocampal CA1 pyramidal neurons and that this effect was mainly mediated by localized downregulation of A-type K+ channel function. Thus, dendritic plasticity might be used to store recent experience in individual branches of the dendritic arbor.</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/OM3UKfZbM40" height="1" width="1"/>]]></content:encoded>
<dc:title>Experience-dependent compartmentalized dendritic plasticity in rat hippocampal CA1 pyramidal neurons</dc:title>
<dc:creator>Judit K Makara</dc:creator>
<dc:creator>Attila Losonczy</dc:creator>
<dc:creator>Quan Wen</dc:creator>
<dc:creator>Jeffrey C Magee</dc:creator>
<dc:identifier>doi:10.1038/nn.2428</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-08</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-08</prism:publicationDate>
<prism:doi>10.1038/nn.2428</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2428</prism:url>
<prism:section>Brief Communication</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2428</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2440">
<title>Self-generated theta oscillations in the hippocampus</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/R20kCAKzP7I/nn.2440</link>
<description>Although numerous in vivo studies have suggested that hippocampal theta oscillations are generated by the extrinsic medial septal input, theoretical studies have suggested that the hippocampus has the minimal feedback circuitry necessary to intrinsically generate its own theta rhythm. Here, Goutagny et al. directly demonstrate such oscillation independently of external inputs.</description>
<content:encoded><![CDATA[

<p>
<b>Self-generated theta oscillations in the hippocampus</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2440">doi:10.1038/nn.2440</a>
</p>
<p>Authors: Romain Goutagny, Jesse Jackson &amp; Sylvain Williams</p>
<p>Hippocampal theta rhythm is crucial for spatial memory and is thought to be generated by extrinsic inputs. In contrast, using a complete rat hippocampus in vitro, we found several intrinsic, atropine-resistant theta generators in CA1. These oscillators were organized along the septotemporal axis and arose independently from CA3. Our results suggest that CA1 theta rhythm can emerge from the coupling of multiple autonomous hippocampal theta oscillators.</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/R20kCAKzP7I" height="1" width="1"/>]]></content:encoded>
<dc:title>Self-generated theta oscillations in the hippocampus</dc:title>
<dc:creator>Romain Goutagny</dc:creator>
<dc:creator>Jesse Jackson</dc:creator>
<dc:creator>Sylvain Williams</dc:creator>
<dc:identifier>doi:10.1038/nn.2440</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-01</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:doi>10.1038/nn.2440</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2440</prism:url>
<prism:section>Brief Communication</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2440</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2411">
<title>The pathways of interoceptive awareness</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/VJEhIdY6Nhw/nn.2411</link>
<description>Studying a patient with selective damage to the insular and anterior cingulate cortex, the current study finds that these regions are not necessary for interoceptive awareness of one's own heartbeat, but the primary somatosensory cortex is required for such self-awareness.</description>
<content:encoded><![CDATA[

<p>
<b>The pathways of interoceptive awareness</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2411">doi:10.1038/nn.2411</a>
</p>
<p>Authors: Sahib S Khalsa, David Rudrauf, Justin S Feinstein &amp; Daniel Tranel</p>
<p>A network of cortical brain regions, including the insula and anterior cingulate cortex (ACC), has been proposed as the critical and sole substrate for interoceptive awareness. Combining lesion and pharmacological approaches in humans, we found that the insula and ACC were not critical for awareness of heartbeat sensations. Instead, this awareness was mediated by both somatosensory afferents from the skin and a network that included the insula and ACC. Together, these pathways enable the core human experience of the cardiovascular state of the body.</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/VJEhIdY6Nhw" height="1" width="1"/>]]></content:encoded>
<dc:title>The pathways of interoceptive awareness</dc:title>
<dc:creator>Sahib S Khalsa</dc:creator>
<dc:creator>David Rudrauf</dc:creator>
<dc:creator>Justin S Feinstein</dc:creator>
<dc:creator>Daniel Tranel</dc:creator>
<dc:identifier>doi:10.1038/nn.2411</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-01</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:doi>10.1038/nn.2411</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2411</prism:url>
<prism:section>Brief Communication</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2411</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2433">
<title>Amyloid-β as a positive endogenous regulator of release probability at hippocampal synapses</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/K9mO3tOjShU/nn.2433</link>
<description>Even without the symptoms of Alzheimer's disease, normal brain releases a small amount of amyloid-β peptide (Aβ). Abramov and colleagues now show that endogenous Aβ that is produced and released from presynaptic terminals can alter synaptic transmission and short-term plasticity.</description>
<content:encoded><![CDATA[

<p>
<b>Amyloid-&#946; as a positive endogenous regulator of release probability at hippocampal synapses</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2433">doi:10.1038/nn.2433</a>
</p>
<p>Authors: Efrat Abramov, Iftach Dolev, Hilla Fogel, Giuseppe D Ciccotosto, Eyal Ruff &amp; Inna Slutsky</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/K9mO3tOjShU" height="1" width="1"/>]]></content:encoded>
<dc:title>Amyloid-β as a positive endogenous regulator of release probability at hippocampal synapses</dc:title>
<dc:creator>Efrat Abramov</dc:creator>
<dc:creator>Iftach Dolev</dc:creator>
<dc:creator>Hilla Fogel</dc:creator>
<dc:creator>Giuseppe D Ciccotosto</dc:creator>
<dc:creator>Eyal Ruff</dc:creator>
<dc:creator>Inna Slutsky</dc:creator>
<dc:identifier>doi:10.1038/nn.2433</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-22</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-22</prism:publicationDate>
<prism:doi>10.1038/nn.2433</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2433</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2433</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2452">
<title>Structural requirements for the activation of vomeronasal sensory neurons by MHC peptides</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/_o8bCRXJ2D0/nn.2452</link>
<description>Major histocompatibility complex peptides function as olfactory cues for vomeronasal sensory neurons (VSNs) in the mammalian nose. Here, the authors report that individual VSNs expressing the receptor gene V2r1b have broad peptide responsiveness, but sufficient specificity to distinguish peptides differing by a single amino acid residue. Furthermore, they find that targeted disruption of V2r1b eliminates the VSN peptide response.</description>
<content:encoded><![CDATA[

<p>
<b>Structural requirements for the activation of vomeronasal sensory neurons by MHC peptides</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2452">doi:10.1038/nn.2452</a>
</p>
<p>Authors: Trese Leinders-Zufall, Tomohiro Ishii, Peter Mombaerts, Frank Zufall &amp; Thomas Boehm</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/_o8bCRXJ2D0" height="1" width="1"/>]]></content:encoded>
<dc:title>Structural requirements for the activation of vomeronasal sensory neurons by MHC peptides</dc:title>
<dc:creator>Trese Leinders-Zufall</dc:creator>
<dc:creator>Tomohiro Ishii</dc:creator>
<dc:creator>Peter Mombaerts</dc:creator>
<dc:creator>Frank Zufall</dc:creator>
<dc:creator>Thomas Boehm</dc:creator>
<dc:identifier>doi:10.1038/nn.2452</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-22</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-22</prism:publicationDate>
<prism:doi>10.1038/nn.2452</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2452</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2452</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2438">
<title>Nardilysin regulates axonal maturation and myelination in the central and peripheral nervous system</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/BES-Qae4LgE/nn.2438</link>
<description>Nardilysin (NRDc) enhances the shedding of ectodomains from neuronal membrane proteins. The null mutant described here reveals that nardilysin is necessary for myelination in both central and peripheral nervous system.</description>
<content:encoded><![CDATA[

<p>
<b>Nardilysin regulates axonal maturation and myelination in the central and peripheral nervous system</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2438">doi:10.1038/nn.2438</a>
</p>
<p>Authors: Mikiko Ohno, Yoshinori Hiraoka, Tatsuhiko Matsuoka, Hidekazu Tomimoto, Keizo Takao, Tsuyoshi Miyakawa, Naoko Oshima, Hiroshi Kiyonari, Takeshi Kimura, Toru Kita &amp; Eiichiro Nishi</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/BES-Qae4LgE" height="1" width="1"/>]]></content:encoded>
<dc:title>Nardilysin regulates axonal maturation and myelination in the central and peripheral nervous system</dc:title>
<dc:creator>Mikiko Ohno</dc:creator>
<dc:creator>Yoshinori Hiraoka</dc:creator>
<dc:creator>Tatsuhiko Matsuoka</dc:creator>
<dc:creator>Hidekazu Tomimoto</dc:creator>
<dc:creator>Keizo Takao</dc:creator>
<dc:creator>Tsuyoshi Miyakawa</dc:creator>
<dc:creator>Naoko Oshima</dc:creator>
<dc:creator>Hiroshi Kiyonari</dc:creator>
<dc:creator>Takeshi Kimura</dc:creator>
<dc:creator>Toru Kita</dc:creator>
<dc:creator>Eiichiro Nishi</dc:creator>
<dc:identifier>doi:10.1038/nn.2438</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-22</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-22</prism:publicationDate>
<prism:doi>10.1038/nn.2438</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2438</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2438</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2447">
<title>Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/UZ89bIRAwis/nn.2447</link>
<description>Nakazawa and colleagues describe a mouse strain in which the NR1 subunit of the NMDA receptor is selectively eliminated in cortical and hippocampal interneurons in early postnatal development. These mice have several behavioral deficits that are consistent with the theory that GABAergic dysfunction contributes to the pathology of several psychiatric disorders, including schizophrenia.</description>
<content:encoded><![CDATA[

<p>
<b>Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2447">doi:10.1038/nn.2447</a>
</p>
<p>Authors: Juan E Belforte, Veronika Zsiros, Elyse R Sklar, Zhihong Jiang, Gu Yu, Yuqing Li, Elizabeth M Quinlan &amp; Kazu Nakazawa</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/UZ89bIRAwis" height="1" width="1"/>]]></content:encoded>
<dc:title>Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes</dc:title>
<dc:creator>Juan E Belforte</dc:creator>
<dc:creator>Veronika Zsiros</dc:creator>
<dc:creator>Elyse R Sklar</dc:creator>
<dc:creator>Zhihong Jiang</dc:creator>
<dc:creator>Gu Yu</dc:creator>
<dc:creator>Yuqing Li</dc:creator>
<dc:creator>Elizabeth M Quinlan</dc:creator>
<dc:creator>Kazu Nakazawa</dc:creator>
<dc:identifier>doi:10.1038/nn.2447</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-15</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-15</prism:publicationDate>
<prism:doi>10.1038/nn.2447</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2447</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2447</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2439">
<title>Attention improves performance primarily by reducing interneuronal correlations</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/QmScB4LxYO0/nn.2439</link>
<description>Previous work has suggested that visual attention improves behavioral performance by increasing the firing rates of individual sensory neurons. Recording from populations of neurons in monkey visual area V4, this study finds that most of the attentional improvement in the population signal results from decreases in interneuronal correlations.</description>
<content:encoded><![CDATA[

<p>
<b>Attention improves performance primarily by reducing interneuronal correlations</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2439">doi:10.1038/nn.2439</a>
</p>
<p>Authors: Marlene R Cohen &amp; John H R Maunsell</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/QmScB4LxYO0" height="1" width="1"/>]]></content:encoded>
<dc:title>Attention improves performance primarily by reducing interneuronal correlations</dc:title>
<dc:creator>Marlene R Cohen</dc:creator>
<dc:creator>John H R Maunsell</dc:creator>
<dc:identifier>doi:10.1038/nn.2439</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-15</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-15</prism:publicationDate>
<prism:doi>10.1038/nn.2439</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2439</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2439</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2442">
<title>Leucine-rich repeat transmembrane proteins instruct discrete dendrite targeting in an olfactory map</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/_WffCHGousU/nn.2442</link>
<description>In Drosophila, the connections between olfactory receptor neurons and projection neurons are highly specific. Here, the authors report that two leucine-rich repeat transmembrane proteins (Capricious and Tartan) serve as a mechanism for projection neuron dendrite targeting in the olfactory map.</description>
<content:encoded><![CDATA[

<p>
<b>Leucine-rich repeat transmembrane proteins instruct discrete dendrite targeting in an olfactory map</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2442">doi:10.1038/nn.2442</a>
</p>
<p>Authors: Weizhe Hong, Haitao Zhu, Christopher J Potter, Gabrielle Barsh, Mitsuhiko Kurusu, Kai Zinn &amp; Liqun Luo</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/_WffCHGousU" height="1" width="1"/>]]></content:encoded>
<dc:title>Leucine-rich repeat transmembrane proteins instruct discrete dendrite targeting in an olfactory map</dc:title>
<dc:creator>Weizhe Hong</dc:creator>
<dc:creator>Haitao Zhu</dc:creator>
<dc:creator>Christopher J Potter</dc:creator>
<dc:creator>Gabrielle Barsh</dc:creator>
<dc:creator>Mitsuhiko Kurusu</dc:creator>
<dc:creator>Kai Zinn</dc:creator>
<dc:creator>Liqun Luo</dc:creator>
<dc:identifier>doi:10.1038/nn.2442</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-15</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-15</prism:publicationDate>
<prism:doi>10.1038/nn.2442</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2442</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2442</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2446">
<title>Glial precursors clear sensory neuron corpses during development via Jedi-1, an engulfment receptor</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/4qBpPM2jNfQ/nn.2446</link>
<description>During development of the peripheral ganglia, 50% of neurons die by apoptosis. This study finds that satellite glial cell precursors clear these neuronal corpses in developing dorsal root ganglia and identifies some of the molecular components involved in this phagocytosis.</description>
<content:encoded><![CDATA[

<p>
<b>Glial precursors clear sensory neuron corpses during development via Jedi-1, an engulfment receptor</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2446">doi:10.1038/nn.2446</a>
</p>
<p>Authors: Hsiao-Huei Wu, Elena Bellmunt, Jami L Scheib, Victor Venegas, Cornelia Burkert, Louis F Reichardt, Zheng Zhou, Isabel Fari&#241;as &amp; Bruce D Carter</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/4qBpPM2jNfQ" height="1" width="1"/>]]></content:encoded>
<dc:title>Glial precursors clear sensory neuron corpses during development via Jedi-1, an engulfment receptor</dc:title>
<dc:creator>Hsiao-Huei Wu</dc:creator>
<dc:creator>Elena Bellmunt</dc:creator>
<dc:creator>Jami L Scheib</dc:creator>
<dc:creator>Victor Venegas</dc:creator>
<dc:creator>Cornelia Burkert</dc:creator>
<dc:creator>Louis F Reichardt</dc:creator>
<dc:creator>Zheng Zhou</dc:creator>
<dc:creator>Isabel Fariñas</dc:creator>
<dc:creator>Bruce D Carter</dc:creator>
<dc:identifier>doi:10.1038/nn.2446</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-15</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-15</prism:publicationDate>
<prism:doi>10.1038/nn.2446</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2446</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2446</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2437">
<title>Vascular niche factor PEDF modulates Notch-dependent stemness in the adult subependymal zone</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/qd_WIsgwV24/nn.2437</link>
<description>Notch signaling is essential for the maintenance of adult neural stem cells in vivo. Here, Andreu-Agulló and colleagues show that PEDF, released from endothelial cells, enhances Notch signaling in the mouse subependymal zone by inactivating a repressor of Notch target genes.</description>
<content:encoded><![CDATA[

<p>
<b>Vascular niche factor PEDF modulates Notch-dependent stemness in the adult subependymal zone</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2437">doi:10.1038/nn.2437</a>
</p>
<p>Authors: Celia Andreu-Agull&#243;, Jos&#233; Manuel Morante-Redolat, Ana C Delgado &amp; Isabel Fari&#241;as</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/qd_WIsgwV24" height="1" width="1"/>]]></content:encoded>
<dc:title>Vascular niche factor PEDF modulates Notch-dependent stemness in the adult subependymal zone</dc:title>
<dc:creator>Celia Andreu-Agulló</dc:creator>
<dc:creator>José Manuel Morante-Redolat</dc:creator>
<dc:creator>Ana C Delgado</dc:creator>
<dc:creator>Isabel Fariñas</dc:creator>
<dc:identifier>doi:10.1038/nn.2437</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-08</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-08</prism:publicationDate>
<prism:doi>10.1038/nn.2437</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2437</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2437</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2431">
<title>Microcircuitry coordination of cortical motor information in self-initiation of voluntary movements</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/32riXoW0q1A/nn.2431</link>
<description>Systematically monitoring the activities of various cortical pyramidal neurons and interneurons during different stages of locomotion, the authors characterize differential firing activities of motor cortex microcircuitry in behaving, head-restraint rats that were trained to push, pull or hold a lever for reward.</description>
<content:encoded><![CDATA[

<p>
<b>Microcircuitry coordination of cortical motor information in self-initiation of voluntary movements</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2431">doi:10.1038/nn.2431</a>
</p>
<p>Authors: Yoshikazu Isomura, Rie Harukuni, Takashi Takekawa, Hidenori Aizawa &amp; Tomoki Fukai</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/32riXoW0q1A" height="1" width="1"/>]]></content:encoded>
<dc:title>Microcircuitry coordination of cortical motor information in self-initiation of voluntary movements</dc:title>
<dc:creator>Yoshikazu Isomura</dc:creator>
<dc:creator>Rie Harukuni</dc:creator>
<dc:creator>Takashi Takekawa</dc:creator>
<dc:creator>Hidenori Aizawa</dc:creator>
<dc:creator>Tomoki Fukai</dc:creator>
<dc:identifier>doi:10.1038/nn.2431</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-08</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-08</prism:publicationDate>
<prism:doi>10.1038/nn.2431</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2431</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2431</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2436">
<title>Dynamic DNA methylation programs persistent adverse effects of early-life stress</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/qFpQmcFBGDE/nn.2436</link>
<description>Severe stress in early childhood can increase an individual's vulnerability to depression later in life. This study found that early-life stress in mice resulted in persistent elevation of the stress hormone arginine vasopressin (AVP), which was caused by persistent hypomethylation of CpG islands in the Avp promoter in the hypothalamus.</description>
<content:encoded><![CDATA[

<p>
<b>Dynamic DNA methylation programs persistent adverse effects of early-life stress</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2436">doi:10.1038/nn.2436</a>
</p>
<p>Authors: Chris Murgatroyd, Alexandre V Patchev, Yonghe Wu, Vincenzo Micale, Yvonne Bockm&#252;hl, Dieter Fischer, Florian Holsboer, Carsten T Wotjak, Osborne F X Almeida &amp; Dietmar Spengler</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/qFpQmcFBGDE" height="1" width="1"/>]]></content:encoded>
<dc:title>Dynamic DNA methylation programs persistent adverse effects of early-life stress</dc:title>
<dc:creator>Chris Murgatroyd</dc:creator>
<dc:creator>Alexandre V Patchev</dc:creator>
<dc:creator>Yonghe Wu</dc:creator>
<dc:creator>Vincenzo Micale</dc:creator>
<dc:creator>Yvonne Bockmühl</dc:creator>
<dc:creator>Dieter Fischer</dc:creator>
<dc:creator>Florian Holsboer</dc:creator>
<dc:creator>Carsten T Wotjak</dc:creator>
<dc:creator>Osborne F X Almeida</dc:creator>
<dc:creator>Dietmar Spengler</dc:creator>
<dc:identifier>doi:10.1038/nn.2436</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-08</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-08</prism:publicationDate>
<prism:doi>10.1038/nn.2436</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2436</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2436</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2416">
<title>Adult generation of glutamatergic olfactory bulb interneurons</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/TZNzNRkbX2w/nn.2416</link>
<description>Neural stem cells in the adult mouse SVZ are thought to only generate GABAergic olfactory bulb interneurons. This study reports that a dorsal region of the adult SVZ gives rise to a glutamatergic type of olfactory bulb neurons. These newborn glutamatergic neurons can be diverted to migrate into the cortex towards an injury, possibly contributing to repair.</description>
<content:encoded><![CDATA[

<p>
<b>Adult generation of glutamatergic olfactory bulb interneurons</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2416">doi:10.1038/nn.2416</a>
</p>
<p>Authors: Monika S Brill, Jovica Ninkovic, Eleanor Winpenny, Rebecca D Hodge, Ilknur Ozen, Roderick Yang, Alexandra Lepier, Sergio Gasc&#243;n, Ferenc Erdelyi, Gabor Szabo, Carlos Parras, Francois Guillemot, Michael Frotscher, Benedikt Berninger, Robert F Hevner, Olivier Raineteau &amp; Magdalena G&#246;tz</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/TZNzNRkbX2w" height="1" width="1"/>]]></content:encoded>
<dc:title>Adult generation of glutamatergic olfactory bulb interneurons</dc:title>
<dc:creator>Monika S Brill</dc:creator>
<dc:creator>Jovica Ninkovic</dc:creator>
<dc:creator>Eleanor Winpenny</dc:creator>
<dc:creator>Rebecca D Hodge</dc:creator>
<dc:creator>Ilknur Ozen</dc:creator>
<dc:creator>Roderick Yang</dc:creator>
<dc:creator>Alexandra Lepier</dc:creator>
<dc:creator>Sergio Gascón</dc:creator>
<dc:creator>Ferenc Erdelyi</dc:creator>
<dc:creator>Gabor Szabo</dc:creator>
<dc:creator>Carlos Parras</dc:creator>
<dc:creator>Francois Guillemot</dc:creator>
<dc:creator>Michael Frotscher</dc:creator>
<dc:creator>Benedikt Berninger</dc:creator>
<dc:creator>Robert F Hevner</dc:creator>
<dc:creator>Olivier Raineteau</dc:creator>
<dc:creator>Magdalena Götz</dc:creator>
<dc:identifier>doi:10.1038/nn.2416</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-01</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:doi>10.1038/nn.2416</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2416</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2416</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2415">
<title>A genetic pathway composed of Sox14 and Mical governs severing of dendrites during pruning</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/ceTiEqm8Pcw/nn.2415</link>
<description>Certain Drosophila dendrites undergo major remodeling during metamorphosis. This study shows that the severing of larval dendrites, which is the first step of remodeling, depends on the upregulation of the cytoskeleton-binding protein Mical by the transcription factor Sox14.</description>
<content:encoded><![CDATA[

<p>
<b>A genetic pathway composed of Sox14 and Mical governs severing of dendrites during pruning</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2415">doi:10.1038/nn.2415</a>
</p>
<p>Authors: Daniel Kirilly, Ying Gu, Yafen Huang, Zhuhao Wu, Arash Bashirullah, Boon Chuan Low, Alex L Kolodkin, Hongyan Wang &amp; Fengwei Yu</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/ceTiEqm8Pcw" height="1" width="1"/>]]></content:encoded>
<dc:title>A genetic pathway composed of Sox14 and Mical governs severing of dendrites during pruning</dc:title>
<dc:creator>Daniel Kirilly</dc:creator>
<dc:creator>Ying Gu</dc:creator>
<dc:creator>Yafen Huang</dc:creator>
<dc:creator>Zhuhao Wu</dc:creator>
<dc:creator>Arash Bashirullah</dc:creator>
<dc:creator>Boon Chuan Low</dc:creator>
<dc:creator>Alex L Kolodkin</dc:creator>
<dc:creator>Hongyan Wang</dc:creator>
<dc:creator>Fengwei Yu</dc:creator>
<dc:identifier>doi:10.1038/nn.2415</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-01</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:doi>10.1038/nn.2415</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2415</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2415</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nn.2441">
<title>Input normalization by global feedforward inhibition expands cortical dynamic range</title>
<link>http://feeds.nature.com/~r/neuro/rss/aop/~3/q26gFfUITYA/nn.2441</link>
<description>The cortex is sensitive to weak stimuli, but also responds to stronger inputs without saturating. In this study, Scanziani and colleagues find some of the circuits that enable neuronal populations to respond to a wide range of input strengths.</description>
<content:encoded><![CDATA[

<p>
<b>Input normalization by global feedforward inhibition expands cortical dynamic range</b>
</p>
<p>Nature Neuroscience. <a href="http://dx.doi.org/10.1038/nn.2441">doi:10.1038/nn.2441</a>
</p>
<p>Authors: Fr&#233;d&#233;ric Pouille, Antonia Marin-Burgin, Hillel Adesnik, Bassam V Atallah &amp; Massimo Scanziani</p>
<img src="http://feeds.feedburner.com/~r/neuro/rss/aop/~4/q26gFfUITYA" height="1" width="1"/>]]></content:encoded>
<dc:title>Input normalization by global feedforward inhibition expands cortical dynamic range</dc:title>
<dc:creator>Frédéric Pouille</dc:creator>
<dc:creator>Antonia Marin-Burgin</dc:creator>
<dc:creator>Hillel Adesnik</dc:creator>
<dc:creator>Bassam V Atallah</dc:creator>
<dc:creator>Massimo Scanziani</dc:creator>
<dc:identifier>doi:10.1038/nn.2441</dc:identifier>
<dc:source>Nature Neuroscience</dc:source>
<dc:date>2009-11-01</dc:date>
<prism:publicationName>Nature Neuroscience</prism:publicationName>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:doi>10.1038/nn.2441</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nn.2441</prism:url>
<prism:section>Article</prism:section>
<prism:startingPage />
<prism:endingPage />
<feedburner:origLink>http://dx.doi.org/10.1038/nn.2441</feedburner:origLink></item>
</rdf:RDF>
