http://www.biomedcentral.com/bmcneurosci/ The editor's pick of recent articles published by BMC Neuroscience 2013-03-04T00:00:00Z Background: Post-stroke hyperglycemia appears to be associated with poor outcome from stroke, greater mortality, and reduced functional recovery. Focal cerebral ischemia data support that neural stem cells (NSCs) play an important role in post-ischemic repair. Here we sought to evaluate the negative effects of hyperglycemia on the cellular biology of NSCs following anoxia, and to test whether high glucose affects NSC recovery from ischemic injury. Results: In this study, we used immortalized adult neural stem cells lines and we induced in vitro ischemia by 6 h oxygen and glucose deprivation (OGD) in an anaerobic incubator. Reperfusion was performed by returning cells to normoxic conditions and the cells were then incubated in experimental medium with various concentrations of glucose (17.5, 27.75, 41.75, and 83.75 mM) for 24 h. We found that high glucose (≥27.75 mM) exposure induced apoptosis of NSCs in a dose-dependent manner after exposure to OGD, using an Annexin V/PI apoptosis detection kit. The cell viability and proliferative activity of NSCs following OGD in vitro, evaluated with both a Cell Counting kit-8 (CCK-8) assay and a 5-ethynyl-2’-deoxyuridine (EdU) incorporation assay, were inhibited by high glucose exposure. Cell cycle analysis showed that high glucose exposure increased the percentage of cells in G0/G1-phase, and reduced the percentage of cells in S-phase. Furthermore, high glucose exposure was found to significantly induce the activation of c-Jun N-terminal protein kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) and suppress extracellular signal-regulated kinase 1/2 (ERK1/2) activity. Conclusions: Our results demonstrate that high glucose induces apoptosis and inhibits proliferation of NSCs following OGD in vitro, which may be associated with the activation of JNK/p38 MAPK pathways and the delay of G1-S transition in the cells. http://www.biomedcentral.com/1471-2202/14/24 Jian Chen Yang Guo Wei Cheng Ruiqing Chen Tianzhu Liu Zhenzhou Chen Sheng Tan BMC Neuroscience 2013, 14:24 2013-03-04T00:00:00Z 10.1186/1471-2202-14-24 Post-stroke hyperglycemia affects NSCs <p>Post-ischemic hyperglycemia induces cell death and inhibits proliferation of neuronal stem cells (NSCs), which may be related to the poorer outcome experienced by patients who have high glucose levels after a stroke.</p> /content/figures/1471-2202-14-24-toc.gif BMC Neuroscience 1471-2202 14 24 2013-03-04T00:00:00Z XML Background: A large number of invertebrate models, including the snail Helix, emerged as particularly suitable tools for investigating the formation of synapses and the specificity of neuronal connectivity. Helix neurons can be individually identified and isolated in cell culture, showing well-conserved size, position, biophysical properties, synaptic connections, and physiological functions. Although we previously showed the potential usefulness of Helix polysynaptic circuits, a full characterization of synaptic connectivity and its dynamics during network development has not been performed. Results: In this paper, we systematically investigated the in vitro formation of polysynaptic circuits, among Helix B2 and the serotonergic C1 neurons, from a morphological and functional point of view. Since these cells are generally silent in culture, networks were chemically stimulated with either high extracellular potassium concentrations or, alternatively, serotonin. Potassium induced a transient depolarization of all neurons. On the other hand, we found prolonged firing activity, selectively maintained following the first serotonin application. Statistical analysis revealed no significant changes in neuronal dynamics during network development. Moreover, we demonstrated that the cell-selective effect of serotonin was also responsible for short-lasting alterations in C1 excitability, without long-term rebounds.Estimation of the functional connections by means of cross-correlation analysis revealed that networks under elevated KCl concentrations exhibited strongly correlated signals with short latencies (about 5 ms), typical of electrically coupled cells. Conversely, neurons treated with serotonin were weakly connected with longer latencies (exceeding 20 ms) between the interacting neurons. Finally, we clearly demonstrated that these two types of correlations (in terms of strength/latency) were effectively related to the presence of electrical or chemical connections, by comparing Micro-Electrode Array (MEA) signal traces with intracellularly recorded cell pairs. Conclusions: Networks treated with either potassium or serotonin were predominantly interconnected through electrical or chemical connections, respectively. Furthermore, B2 response and short-term increase in C1 excitability induced by serotonin is sufficient to trigger spontaneous activity with chemical connections, an important requisite for long-term maintenance of firing activity. http://www.biomedcentral.com/1471-2202/14/22 Paolo Massobrio Carlo NG Giachello Mirella Ghirardi Sergio Martinoia BMC Neuroscience 2013, 14:22 2013-02-25T00:00:00Z 10.1186/1471-2202-14-22 Snail polysynaptic circuits characterized <p>Neurons isolated from the Helix snail can be used to investigate the formation of polysynaptic networks, with different chemical treatments causing the formation of either electric or chemical connections, and serotonin application leading to spontaneous firing activity.</p> /content/figures/1471-2202-14-22-toc.gif BMC Neuroscience 1471-2202 14 22 2013-02-25T00:00:00Z XML Background: The neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood–brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5. Here, we evaluated the role of CCR5 on traffic of leukocytes in the brain microvasculature, cellular and cytokines profile in a severe form of herpetic encephalitis. Results: Wild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice. Conclusions: These results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host. http://www.biomedcentral.com/1471-2202/14/19 Márcia Carvalho Vilela Graciela Kunrath Lima David Henrique Rodrigues Norinne Lacerda-Queiroz Vinicius Sousa Pietra Pedroso Aline Silva Miranda Milene Alvarenga Rachid Erna Geessien Kroon Marco Antônio Campos Mauro Martins Teixeira Johann Sellner Antonio Lucio Teixeira BMC Neuroscience 2013, 14:19 2013-02-07T00:00:00Z 10.1186/1471-2202-14-19 Chemokine receptor has role in herpetic encephalitis <p>The absence of the chemokine receptor CCR5 in mice inoculated with herpes simplex virus 1 leads to a lower viral load and high neutrophil recruitment, thought to play a role in the pathogenesis of neuroaxonal damage in herpetic encephalitis.</p> /content/figures/1471-2202-14-19-toc.gif BMC Neuroscience 1471-2202 14 19 2013-02-07T00:00:00Z XML Background: Anti-NMDA-encephalitis is caused by antibodies against the N-methyl-D-aspartate receptor (NMDAR) and characterized by a severe encephalopathy with psychosis, epileptic seizures and autonomic disturbances. It predominantly occurs in young women and is associated in 59% with an ovarian teratoma. Results: We describe effects of cerebrospinal fluid (CSF) from an anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis patient on in vitro neuronal network activity (ivNNA). In vitro NNA of dissociated primary rat cortical populations was recorded by the microelectrode array (MEA) system.The 23-year old patient was severely affected but showed an excellent recovery following multimodal immunomodulatory therapy and removal of an ovarian teratoma. Patient CSF (pCSF) taken during the initial weeks after disease onset suppressed global spike- and burst rates of ivNNA in contrast to pCSF sampled after clinical recovery and decrease of NMDAR antibody titers. The synchrony of pCSF-affected ivNNA remained unaltered during the course of the disease. Conclusion: Patient CSF directly suppresses global activity of neuronal networks recorded by the MEA system. In contrast, pCSF did not regulate the synchrony of ivNNA suggesting that NMDAR antibodies selectively regulate distinct parameters of ivNNA while sparing their functional connectivity. Thus, assessing ivNNA could represent a new technique to evaluate functional consequences of autoimmune encephalitis-related CSF changes. http://www.biomedcentral.com/1471-2202/14/17 Sabine U Jantzen Stefano Ferrea Claudia Wach Kim Quasthoff Sebastian Illes Dag Scherfeld Hans-Peter Hartung Rüdiger J Seitz Marcel Dihné BMC Neuroscience 2013, 14:17 2013-02-05T00:00:00Z 10.1186/1471-2202-14-17 Evaluating anti-NMDA-encephalitis effects <p>Cerebrospinal fluid from a patient with anti-NMDA-encephalitis suppresses the activity of in vitro neuronal network activity in cortical rat neurons grown on microelectrode arrays, potentially offering a new technique to evaluate the functional consequences of the disease.</p> /content/figures/1471-2202-14-17-toc.gif BMC Neuroscience 1471-2202 14 17 2013-02-05T00:00:00Z XML Background: The purpose of this study was to examine task-related changes in prefrontal cortex (PFC) activity during a dual-task in both healthy young and older adults and compare patterns of activation between the age groups. We also sought to determine whether brain activation during a dual-task relates to executive/attentional function and how measured factors associated with both of these functions vary between older and younger adults. Results: Thirty-five healthy volunteers (20 young and 15 elderly) participated in this study. Near-infrared spectroscopy (NIRS) was employed to measure PFC activation during a single-task (performing calculations or stepping) and dual-task (performing both single-tasks at once). Cognitive function was assessed in the older patients with the Trail-making test part B (TMT-B). Major outcomes were task performance, brain activation during task (oxygenated haemoglobin: Oxy-Hb) measured by NIRS, and TMT-B score. Mixed ANOVAs were used to compare task factors and age groups in task performance. Mixed ANOVAs also compared task factors, age group and time factors in task-induced changes in measured Oxy-Hb. Among the older participants, correlations between the TMT-B score and Oxy-Hb values measured in each single-task and in the dual-task were examined using a Pearson correlation coefficient.Oxy-Hb values were significantly increased in both the calculation task and the dual-task within patients in both age groups. However, the Oxy-Hb values associated with there were higher in the older group during the post-task period for the dual-task. Also, there were significant negative correlations between both task-performance accuracy and Oxy-Hb values during the dual-task and participant TMT-B scores. Conclusions: Older adults demonstrated age-specific PFC activation in response to dual-task challenge. There was also a significant negative correlation between PFC activation during dual-task and executive/attentional function. These findings suggest that the high cognitive load induced by dual-task activity generates increased PFC activity in older adults. However, this relationship appeared to be strongest in participants with better baseline attention and executive functions. http://www.biomedcentral.com/1471-2202/14/10 Hironori Ohsugi Shohei Ohgi Kenta Shigemori Eric B Schneider BMC Neuroscience 2013, 14:10 2013-01-18T00:00:00Z 10.1186/1471-2202-14-10 Dual tasks increase PFC activity in older adults <p>When performing physical and mental tasks simultaneously, older adults have higher prefrontal cortex (PFC) activity lasting longer than younger adults, indicating that high cognitive load induced by dual-task activity generates increased PFC activity.</p> /content/figures/1471-2202-14-10-toc.gif BMC Neuroscience 1471-2202 14 10 2013-01-18T00:00:00Z XML