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        <title>BMC Neuroscience - Latest Articles</title>
        <link>http://www.biomedcentral.com/bmcneurosci/</link>
        <description>The latest research articles published by BMC Neuroscience</description>
        <dc:date>2012-05-30T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/55" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/54" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/53" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/52" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/51" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/50" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/49" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/48" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/47" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2202/13/46" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/55">
        <title>Effect of temporal predictability on the neural processing of self-triggered auditory stimulation during vocalization</title>
        <description>Background:
Sensory consequences of our own actions are perceived differently from the sensory stimuli that are generated externally. The present event-related potential (ERP) study examined the neural responses to self-triggered stimulation relative to externally-triggered stimulation as a function of delays between the motor act and the stimulus onset. While sustaining a vowel phonation, subjects clicked a mouse and heard pitch-shift stimuli (PSS) in voice auditory feedback at delays of either 0 ms (predictable) or 500-1000 ms (unpredictable). The motor effect resulting from the mouse click was corrected in the data analyses. For the externally-triggered condition, PSS were delivered by a computer with a delay of 500-1000 ms after the vocal onset.
Results:
As compared to unpredictable externally-triggered PSS, P2 responses to predictable self-triggered PSS were significantly suppressed, whereas an enhancement effect for P2 responses was observed when the timing of self-triggered PSS was unpredictable.
Conclusions:
These findings demonstrate the effect of the temporal predictability of stimulus delivery with respect to the motor act on the neural responses to self-triggered stimulation. Responses to self-triggered stimulation were suppressed or enhanced compared with the externally-triggered stimulation when the timing of stimulus delivery was predictable or unpredictable. Enhancement effect of unpredictable self-triggered stimulation in the present study supports the idea that sensory suppression of self-produced action may be primarily caused by an accurate prediction of stimulus timing, rather than a movement-related non-specific suppression.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/55</link>
                <dc:creator>Zhaocong Chen</dc:creator>
                <dc:creator>Xi Chen</dc:creator>
                <dc:creator>Peng Liu</dc:creator>
                <dc:creator>Dongfeng Huang</dc:creator>
                <dc:creator>Hanjun Liu</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:55</dc:source>
        <dc:date>2012-05-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2202-13-55</dc:identifier>
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                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>55</prism:startingPage>
        <prism:publicationDate>2012-05-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/54">
        <title>Culture but not gender modulates amygdala
activation during explicit emotion recognition</title>
        <description>Background:
Mounting evidence indicates that humans have significant difficulties in understandingemotional expressions from individuals of different ethnic backgrounds, leading to reducedrecognition accuracy and stronger amygdala activation. However, the impact of gender on thebehavioral and neural reactions during the initial phase of cultural assimilation has not beenaddressed. Therefore, we investigated 24 Asians students (12 females) and 24 age-matchedEuropean students (12 females) during an explicit emotion recognition task, using Caucasianfacial expressions only, on a high-field MRI scanner.
Results:
Analysis of functional data revealed bilateral amygdala activation to emotional expressions inAsian and European subjects. However, in the Asian sample, a stronger response of theamygdala emerged and was paralleled by reduced recognition accuracy, particularly for angrymale faces. Moreover, no significant gender difference emerged. We also observed asignificant inverse correlation between duration of stay and amygdala activation.
Conclusion:
In this study we investigated the &quot;alien-effect&quot; as an initial problem during culturalassimilation and examined this effect on a behavioral and neural level. This study hasrevealed bilateral amygdala activation to emotional expressions in Asian and Europeanfemales and males. In the Asian sample, a stronger response of the amygdala bilaterally wasobserved and this was paralleled by reduced performance, especially for anger and disgustdepicted by male expressions. However, no gender difference occurred. Taken together,while gender exerts only a subtle effect, culture and duration of stay as well as gender ofposer are shown to be relevant factors for emotion processing, influencing not onlybehavioral but also neural responses in female and male immigrants.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/54</link>
                <dc:creator>Birgit Derntl</dc:creator>
                <dc:creator>Ute Habel</dc:creator>
                <dc:creator>Simon Robinson</dc:creator>
                <dc:creator>Christian Windischberger</dc:creator>
                <dc:creator>Ilse Kryspin-Exner</dc:creator>
                <dc:creator>Ruben Gur</dc:creator>
                <dc:creator>Ewald Moser</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:54</dc:source>
        <dc:date>2012-05-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2202-13-54</dc:identifier>
                                <prism:require>/content/figures/1471-2202-13-54-toc.gif</prism:require>
                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>54</prism:startingPage>
        <prism:publicationDate>2012-05-29T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/53">
        <title>Mechanisms of constitutive and ATP-evoked ATP
release in neonatal mouse olfactory epithelium</title>
        <description>Background:
ATP is an extracellular signaling molecule with many ascribed functions in sensory systems,including the olfactory epithelium. The mechanism(s) by which ATP is released in theolfactory epithelium has not been investigated. Quantitative luciferin-luciferase assays wereused to monitor ATP release, and confocal imaging of the fluorescent ATP marker quinacrinewas used to monitor ATP release via exocytosis in Swiss Webster mouse neonatal olfactoryepithelial slices.
Results:
Under control conditions, constitutive release of ATP occurs via exocytosis, hemichannelsand ABC transporters and is inhibited by vesicular fusion inhibitor Clostridium difficile toxinA and hemichannel and ABC transporter inhibitor probenecid. Constitutive ATP release isnegatively regulated by the ATP breakdown product ADP through activation of P2Yreceptors, likely via the cAMP/PKA pathway. In vivo studies indicate that constitutive ATPmay play a role in neuronal homeostasis as inhibition of exocytosis inhibited normalproliferation in the OE. ATP-evoked ATP release is also present in mouse neonatal OE,triggered by several ionotropic P2X purinergic receptor agonists (ATP, alphabetaMeATP and Bz-ATP) and a G protein-coupled P2Y receptor agonist (UTP). Calcium imaging of P2X2-transfected HEK293 &quot;biosensor&quot; cells confirmed the presence of evoked ATP release.Following purinergic receptor stimulation, ATP is released via calcium-dependentexocytosis, activated P2X1,7 receptors, activated P2X7 receptors that form a complex withpannexin channels, or ABC transporters. The ATP-evoked ATP release is inhibited by thepurinergic receptor inhibitor PPADS, Clostridium difficile toxin A and two inhibitors ofpannexin channels: probenecid and carbenoxolone.
Conclusions:
The constitutive release of ATP might be involved in normal cell turn-over or modulation ofodorant sensitivity in physiological conditions. Given the growth-promoting effects of ATP,ATP-evoked ATP release following injury could lead to progenitor cell proliferation,differentiation and regeneration. Thus, understanding mechanisms of ATP release is ofparamount importance to improve our knowledge about tissue homeostasis and post-injuryneuroregeneration. It will lead to development of treatments to restore loss of smell and,when transposed to the central nervous system, improve recovery following central nervoussystem injury.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/53</link>
                <dc:creator>Sebastien Hayoz</dc:creator>
                <dc:creator>Cuihong Jia</dc:creator>
                <dc:creator>Colleen Cosgrove Hegg</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:53</dc:source>
        <dc:date>2012-05-28T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2202-13-53</dc:identifier>
                                <prism:require>/content/figures/1471-2202-13-53-toc.gif</prism:require>
                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>53</prism:startingPage>
        <prism:publicationDate>2012-05-28T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/52">
        <title>Neural activity associated with self-reflection</title>
        <description>Background:
Self-referential cognitions are important for self-monitoring and self-regulation. Previous studies have addressed the neural correlates of self-referential processes in response to or related to external stimuli. We here investigated brain activity associated with a short, exclusively mental process of self-reflection in the absence of external stimuli or behavioural requirements. Healthy subjects reflected either on themselves, a personally known or an unknown person during functional magnetic resonance imaging (fMRI). The reflection period was initialized by a cue and followed by photographs of the respective persons (perception of pictures of oneself or the other person).
Results:
Self-reflection, compared with reflecting on the other persons and to a major part also compared with perceiving photographs of one-self, was associated with more prominent dorsomedial and lateral prefrontal, insular, anterior and posterior cingulate activations. Whereas some of these areas showed activity in the &quot;other&quot;-conditions as well, self-selective characteristics were revealed in right dorsolateral prefrontal and  posterior cingulate cortex for self-reflection; in anterior cingulate cortex for self-perception and in the left inferior parietal lobe for self-reflection and -perception.
Conclusions:
Altogether, cingulate, medial and lateral prefrontal, insular and inferior parietal regions show relevance for self-related cognitions, with in part self-specificity in terms of comparison with the known-, unknown- and perception-conditions. Notably, the results are obtained here without behavioural response supporting the reliability of this methodological approach of applying a solely mental intervention. We suggest considering the reported structures when investigating psychopathologically affected self-related processing.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/52</link>
                <dc:creator>Uwe Herwig</dc:creator>
                <dc:creator>Tina Kaffenberger</dc:creator>
                <dc:creator>Caroline Schell</dc:creator>
                <dc:creator>Lutz Jäncke</dc:creator>
                <dc:creator>Annette Bruehl</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:52</dc:source>
        <dc:date>2012-05-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2202-13-52</dc:identifier>
                                <prism:require>/content/figures/1471-2202-13-52-toc.gif</prism:require>
                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>52</prism:startingPage>
        <prism:publicationDate>2012-05-24T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/51">
        <title>Immunocytochemical Analysis of P2X2 in Rat
Circumvallate Taste Buds</title>
        <description>Background:
Our laboratory has shown that classical synapses and synaptic proteins are associated withType III cells. Yet it is generally accepted that Type II cells transduce bitter, sweet andumami stimuli. No classical synapses, however, have been found associated with Type IIcells. Recent studies indicate that ionotropic purinergic receptors P2X2/P2X3 are present inrodent taste buds. Taste nerve processes express the ionotropic purinergic receptors(P2X2/P2X3). P2X2/P2X3Dbl/ mice are not responsive to sweet, umami and bitter stimuli,and it has been proposed that ATP acts as a neurotransmitter in taste buds. The goal of thepresent study is to learn more about the nature of purinergic contacts in rat circumvallate tastebuds by examining immunoreactivity to antisera directed against the purinergic receptorP2X2.
Results:
P2X2-like immunoreactivity is present in intragemmal nerve processes in rat circumvallatetaste buds. Intense immunoreactivity can also be seen in the subgemmal nerve plexuseslocated below the basal lamina. The P2X2 immunoreactive nerve processes also displaysyntaxin-1-LIR. The immunoreactive nerves are in close contact with the IP3R3-LIR Type IIcells and syntaxin-1-LIR and/or 5-HT-LIR Type III cells. Taste cell synapses are observedonly from Type III taste cells onto P2X2-LIR nerve processes. Unusually large, &quot;atypical&quot;mitochondria in the Type II taste cells are found only at the close appositions with P2X2-LIRnerve processes. P2X2 immunogold particles are concentrated at the membranes of nerveprocesses at the close appositions with taste cells.
Conclusions:
Based on our fluorescence and immunoelectron microscopical studies we believe that bothperigemmal and most all intragemmal nerve processes display P2X2-LIR. Moreover,colloidal gold immunoelectron microscopy indicates that P2X2-LIR in nerve processes isconcentrated at sites of close apposition with Type II cells. This supports the hypothesis thatATP may be a key neurotransmitter in taste transduction and that Type II cells release ATP,activating P2X2 receptors in nerve processes.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/51</link>
                <dc:creator>Ruibiao Yang</dc:creator>
                <dc:creator>Alana Montoya</dc:creator>
                <dc:creator>Amanda Bond</dc:creator>
                <dc:creator>Jenna Walton</dc:creator>
                <dc:creator>John Kinnamon</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:51</dc:source>
        <dc:date>2012-05-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2202-13-51</dc:identifier>
                                <prism:require>/content/figures/1471-2202-13-51-toc.gif</prism:require>
                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>51</prism:startingPage>
        <prism:publicationDate>2012-05-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/50">
        <title>Dose-dependent changes in neuroinflammatory and
arachidonic acid cascade markers with synaptic
marker loss in rat lipopolysaccharide infusion model
of neuroinflammation</title>
        <description>Background:
Neuroinflammation, caused by six days of intracerebroventricular infusion of bacteriallipopolysaccharide (LPS), stimulates rat brain arachidonic acid (AA) metabolism. Themolecular changes associated with increased AA metabolism are not clear. We examinedeffects of a six-day infusion of a low-dose (0.5 ng/h) and a high-dose (250 ng/h) of LPS onneuroinflammatory, AA cascade, and pre- and post-synaptic markers in rat brain. We usedartificial cerebrospinal fluid-infused brains as controls.
Results:
Infusion of low- or high-dose LPS increased brain protein levels of TNFalpha, and iNOS, withoutsignificantly changing GFAP. High-dose LPS infusion upregulated brain protein and mRNAlevels of AA cascade markers (cytosolic cPLA2-IVA, secretory sPLA2-V, cyclooxygenase-2and 5-lipoxygenase), and of transcription factor NF-kappaB p50 DNA binding activity. Both LPSdoses increased cPLA2 and p38 mitogen-activated protein kinase levels, while reducingprotein levels of the pre-synaptic marker, synaptophysin. Post-synaptic markers drebrin andPSD95 protein levels were decreased with high- but not low-dose LPS.
Conclusions:
Chronic LPS infusion has differential effects, depending on dose, on inflammatory, AA andsynaptic markers in rat brain. Neuroinflammation associated with upregulated brain AAmetabolism can lead to synaptic dysfunction.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/50</link>
                <dc:creator>Matthew Kellom</dc:creator>
                <dc:creator>Mireille Basselin</dc:creator>
                <dc:creator>Vasken Keleshian</dc:creator>
                <dc:creator>Mei Chen</dc:creator>
                <dc:creator>Stanley Rapoport</dc:creator>
                <dc:creator>Jagadeesh Rao</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:50</dc:source>
        <dc:date>2012-05-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2202-13-50</dc:identifier>
                                <prism:require>/content/figures/1471-2202-13-50-toc.gif</prism:require>
                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>50</prism:startingPage>
        <prism:publicationDate>2012-05-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/49">
        <title>Emotional event-related potentials are larger to figures than scenes but are similarly reduced by inattention</title>
        <description>Background:
In research on event related potentials (ERP) to emotional pictures, greater attention toemotional than neutral stimuli (i.e., motivated attention) is commonly indexed by twodifference waves between emotional and neutral stimuli: the early posterior negativity (EPN)and the late positive potential (LPP). Evidence suggests that if attention is directed away fromthe pictures, then the emotional effects on EPN and LPP are eliminated. However, a fewstudies have found residual, emotional effects on EPN and LPP. In these studies, pictureswere shown at fixation, and picture composition was that of simple figures rather than that ofcomplex scenes. Because figures elicit larger LPP than do scenes, figures might capture andhold attention more strongly than do scenes. Here, we showed negative and neutral picturesof figures and scenes and tested first, whether emotional effects are larger to figures thanscenes for both EPN and LPP, and second, whether emotional effects on EPN and LPP arereduced less for unattended figures than scenes.
Results:
Emotional effects on EPN and LPP were larger for figures than scenes. When pictures wereunattended, emotional effects on EPN increased for scenes but tended to decrease for figures,whereas emotional effects on LPP decreased similarly for figures and scenes.
Conclusions:
Emotional effects on EPN and LPP were larger for figures than scenes, but these effects didnot resist manipulations of attention more strongly for figures than scenes. These findingsimply that the emotional content captures attention more strongly for figures than scenes, butthat the emotional content does not hold attention more strongly for figures than scenes.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/49</link>
                <dc:creator>Henrik Nordström</dc:creator>
                <dc:creator>Stefan Wiens</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:49</dc:source>
        <dc:date>2012-05-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2202-13-49</dc:identifier>
                                <prism:require>/content/figures/1471-2202-13-49-toc.gif</prism:require>
                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>49</prism:startingPage>
        <prism:publicationDate>2012-05-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2202/13/48">
        <title>Increasing levels of wild-type CREB up-regulates
several activity-regulated inhibitor of death (AID)
genes and promotes neuronal survival</title>
        <description>Background:
CREB (cAMP-response element binding protein) is the prototypical signal-regulatedtranscription factor. In neurons, it is the target of the synaptic activity-induced nuclearcalcium-calcium/calmodulin dependent protein kinase (CaMK) IV signaling pathway thatcontrols the expression of genes important for acquired neuroprotection as well as other longlastingadaptive processes in the nervous system. The function of CREB as a transcriptionalactivator is controlled by its phosphorylation on serine 133, which can be catalyzed byCaMKIV and leads to the recruitment of the co-activator, CREB binding protein (CBP).Activation of CBP function by nuclear calcium-CaMKIV signaling is a second regulatorystep required for CREB/CBP-mediated transcription.
Results:
Here we used recombinant adeno-associated virus (rAAV) to increase the levels of wild typeCREB or to overexpress a mutant version of CREB (mCREB) containing a serine to alaninemutation at position amino acid 133 in mouse hippocampal neurons. Increasing the levels ofCREB was sufficient to boost neuroprotective activity even under basal conditions (i.e., in theabsence of stimulation of synaptic activity). In contrast, overexpression of mCREB increasedcell death. The ratio of phospho(serine 133)CREB to CREB immunoreactivity inunstimulated hippocampal neurons was similar for endogenous CREB and overexpressedwild type CREB and, as expected, dramatically reduced for overexpressed mCREB. A geneexpression analysis revealed that increased expression of CREB but not that of mCREB inhippocampal neurons led to elevated expression levels of bdnf as well as that of severalmembers of a previously characterized set of Activity-regulated Inhibitor of Death (AID)genes, which include atf3, btg2, gadd45beta, and gadd45gamma.
Conclusions:
Our findings indicate that the expression levels of wild type CREB are a critical determinantof the ability of hippocampal neurons to survive harmful conditions. Increasing the levels ofwild type CREB can, even without inducing synaptic activity, increase pro-survival geneexpression and strengthen the neurons&apos; neuroprotective shield. The observed degradation ofCREB protein following NMDA treatment of hippocampal neurons suggests that the knownCREB shut-off associated with extrasynaptic NMDA receptor-induced excitotoxicity isfollowed by CREB proteolysis.</description>
        <link>http://www.biomedcentral.com/1471-2202/13/48</link>
                <dc:creator>Yan-Wei Tan</dc:creator>
                <dc:creator>Sheng-Jia Zhang</dc:creator>
                <dc:creator>Tina Hoffmann</dc:creator>
                <dc:creator>Hilmar Bading</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:48</dc:source>
        <dc:date>2012-05-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2202-13-48</dc:identifier>
                                <prism:require>/content/figures/1471-2202-13-48-toc.gif</prism:require>
                <prism:publicationName>BMC Neuroscience</prism:publicationName>
        <prism:issn>1471-2202</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>48</prism:startingPage>
        <prism:publicationDate>2012-05-18T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <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, null:47</dc:source>
        <dc:date>2012-05-15T00:00:00Z</dc:date>
        <dc:identifier>doi: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>
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        <prism:startingPage>47</prism:startingPage>
        <prism:publicationDate>2012-05-15T00:00:00Z</prism:publicationDate>
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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 Witte</dc:creator>
                <dc:creator>Anja Urbach</dc:creator>
                <dc:source>BMC Neuroscience 2012, null:46</dc:source>
        <dc:date>2012-05-07T00:00:00Z</dc:date>
        <dc:identifier>doi: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>
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        <prism:startingPage>46</prism:startingPage>
        <prism:publicationDate>2012-05-07T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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