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        <title>Editor's picks</title>
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        <description>The editor's pick of recent articles published by BMC Neuroscience</description>
        <dc:date>2012-05-15T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/47" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/46" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/8" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/47">
        <title>Hydrogen-rich saline alleviates early brain injury
via reducing oxidative stress and brain edema
following experimental subarachnoid hemorrhage in
rabbits</title>
        <description>Background:
Increasing experimental and clinical data indicate that early brain injury (EBI) aftersubarachnoid hemorrhage (SAH) largely contributes to unfavorable outcomes, and it has beenproved that EBI following SAH is closely associated with oxidative stress and brain edema.The present study aimed to examine the effect of hydrogen, a mild and selective cytotoxicoxygen radical scavenger, on oxidative stress injury, brain edema and neurology outcomefollowing experimental SAH in rabbit.
Results:
The level of MDA, caspase-12/3 and brain water content increased significantly at 72 hoursafter experimental SAH. Correspondingly, obvious brain injury was found in the SAH groupby terminal deoxynucleotidyl transferase-mediated uridine 5&apos;-triphosphate-biotin nick endlabeling(TUNEL) and Nissl staining. Similar results were found in the SAH + saline group.In contrast, the upregulated level of MDA, caspase-12/3 and brain edema was attenuated andthe brain injury was substantially alleviated in the hydrogen treated rabbits, but theimprovement of neurology outcome was not obvious.
Conclusion:
The results suggest that treatment with hydrogen in experimental SAH rabbits could alleviatebrain injury via decreasing the oxidative stress injury and brain edema. Hence, we concludethat hydrogen possesses the potential to be a novel therapeutic agent for EBI after SAH.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/47</link>
                <dc:creator>Zong Zhuang</dc:creator>
                <dc:creator>Meng-liang Zhou</dc:creator>
                <dc:creator>Wan-chun You</dc:creator>
                <dc:creator>Lin Zhu</dc:creator>
                <dc:creator>Chi-yuan Ma</dc:creator>
                <dc:creator>Xue-jun Sun</dc:creator>
                <dc:creator>Ji-xin Shi</dc:creator>
                <dc:source>BMC Neuroscience 2012, 13:47</dc:source>
        <dc:date>2012-05-15T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2202-13-47</dc:identifier>
                            <dc:title>Hydrogen alleviates early brain injury</dc:title>
                            <dc:description>Early brain injury in rabbits treated with hydrogen-rich saline following subarachnoid hemorrhage is alleviated by decreasing oxidative stress injury and brain edema, suggesting a potential use as a therapeutic agent.</dc:description>
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                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>47</prism:startingPage>
        <prism:publicationDate>2012-05-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
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        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/46">
        <title>Age-dependent kinetics of dentate gyrus neurogenesis in the absence of cyclin D2</title>
        <description>Background:
Adult neurogenesis continuously adds new neurons to the dentate gyrus and the olfactorybulb. It involves the proliferation and subsequent differentiation of neuronal progenitors, andis thus closely linked to the cell cycle machinery. Cell cycle progression is governed by thesuccessive expression, activation and degradation of regulatory proteins. Among them, Dtypecyclins control the exit from the G1 phase of the cell cycle. Cyclin D2 (cD2) has beenshown to be required for the generation of new neurons in the neurogenic niches of the adultbrain. It is differentially expressed during hippocampal development, and adult cD2 knockout (cD2KO) mice virtually lack neurogenesis in the dentate gyrus and olfactory bulb. In thepresent study we examined the dynamics of postnatal and adult neurogenesis in the dentategyrus (DG) of cD2KO mice. Animals were injected with bromodeoxyuridine at seven timepoints during the first 10 months of life and brains were immunohistochemically analyzed fortheir potential to generate new neurons.
Results:
Compared to their WT litters, cD2KO mice had considerably reduced numbers of newly borngranule cells during the postnatal period, with neurogenesis becoming virtually absent aroundpostnatal day 28. This was paralleled by a reduction in granule cell numbers, in the volume ofthe granule cell layer as well as in apoptotic cell death. CD2KO mice did not show any of theage-related changes in neurogenesis and granule cell numbers that were seen in WT litters.
Conclusions:
The present study suggests that hippocampal neurogenesis becomes increasingly dependenton cD2 during early postnatal development. In cD2KO mice, hippocampal neurogenesisceases at a time point at which the tertiary germinative matrix stops proliferating, indicatingthat cD2 becomes an essential requirement for ongoing neurogenesis with the transition fromdevelopmental to adult neurogenesis. Our data further support the notion that adultneurogenesis continuously adds new neurons to the hippocampal network, hence increasingcell density of the DG.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/46</link>
                <dc:creator>Anne Ansorg</dc:creator>
                <dc:creator>Otto W Witte</dc:creator>
                <dc:creator>Anja Urbach</dc:creator>
                <dc:source>BMC Neuroscience 2012, 13:46</dc:source>
        <dc:date>2012-05-07T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2202-13-46</dc:identifier>
                            <dc:title>Adult neurogenesis dependent on cD2</dc:title>
                            <dc:description>From the early post-natal period Cyclin D2 (cD2) knockout  mice show reduced neurogenesis in the dentate gyrus and olfactory bulb, and it is virtually absent by day 28 indicating that cD2 is an essential requirement for ongoing neurogenesis.</dc:description>
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                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>46</prism:startingPage>
        <prism:publicationDate>2012-05-07T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
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        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/8">
        <title>Electrophysiological correlates of associative learning in smokers: a higher-order conditioning experiment</title>
        <description>Background:
Classical conditioning has been suggested to play an important role in the development, maintenance, and relapse of tobacco smoking. Several studies have shown that initially neutral stimuli that are directly paired with smoking are able to elicit conditioned responses. However, there have been few human studies that demonstrate the contribution of higher-order conditioning to smoking addiction, although it is assumed that higher-order conditioning predominates learning in the outside world. In the present study a higher-order conditioning task was designed in which brain responses of smokers and non-smokers were conditioned by pairing smoking-related and neutral stimuli (CS1smoke and CS1neutral) with two geometrical figures (CS2smoke and CS2neutral). ERPs were recorded to all CSs.
Results:
Data showed that the geometrical figure that was paired with smoking stimuli elicited significantly larger P2 and P3 waves than the geometrical figure that was paired with neutral stimuli. During the first half of the experiment this effect was only present in smokers whereas non-smokers displayed no significant differences between both stimuli, indicating that neutral cues paired with motivationally relevant smoking-related stimuli gain more motivational significance even though they were never paired directly with smoking. These conclusions are underscored by self-reported evidence of enhanced second-order conditioning in smokers.
Conclusions:
It can be concluded that smokers show associative learning for higher-order smoking-related stimuli. The present study directly shows the contribution of higher-order conditioning to smoking addiction and is the first to reveal its electrophysiological correlates. Although results are preliminary, they may help in understanding the etiology of smoking addiction and its persistence.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/8</link>
                <dc:creator>Marianne Littel</dc:creator>
                <dc:creator>Ingmar HA Franken</dc:creator>
                <dc:source>BMC Neuroscience 2012, 13:8</dc:source>
        <dc:date>2012-01-11T00:00:00Z</dc:date>
        <dc:identifier>10.1186/1471-2202-13-8</dc:identifier>
                            <dc:title>Smoking-related higher-order conditioning</dc:title>
                            <dc:description>Paired smoking-related and neutral cues elicit enhanced event-related potentials in the brains of smokers compared to non-smokers, providing electrophysiological evidence of higher-order, associative learning which may play a role in addiction.</dc:description>
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                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>13</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2012-01-11T00:00:00Z</prism:publicationDate>
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