http://www.biomedcentral.com/bmcneurosci/ The latest research articles published by BMC Neuroscience 2009-12-04T00:00:00Z This is an RSS newsfeed from BioMed Central It is intended to be used with an RSS reader. For more information about RSS newsfeeds from BioMed Central, visit http://www.biomedcentral.com/info/about/rss/ Background: It has been postulated that exercise-induced activation of brain-derived neurotrophic factor (BDNF) may account for improvement of stepping ability in animals after complete spinal cord transection. As we have shown previously, treadmill locomotor exercise leads to up-regulation of BDNF protein and mRNA in the entire neuronal network of intact spinal cord. The questions arise: (i) how the treadmill locomotor training, supplemented with tail stimulation, affects the expression of molecular correlates of synaptic plasticity in spinal rats, and (ii) if a response is related to BDNF protein level and distribution.We investigated the effect of training in rats spinalized at low thoracic segments on the level and distribution of BDNF immunoreactivity (IR) in ventral quadrants of the lumbar segments, in conjunction with markers of presynaptic terminals, synaptophysin and synaptic zinc. Results: Training improved hindlimb stepping in spinal animals evaluated with modified Basso-Beattie-Bresnahan scale. Grades of spinal trained animals ranged between 5 and 11, whereas those of spinal were between 2 and 4. Functional improvement was associated with changes in presynaptic markers and BDNF distribution. Six weeks after transection, synaptophysin IR was reduced by 18% around the large neurons of lamina IX and training elevated its expression by over 30%. The level of synaptic zinc staining in the ventral horn was unaltered, whereas in ventral funiculi it was decreased by 26% postlesion and tended to normalize after the training. Overall BDNF IR levels in the ventral horn, which were higher by 22% postlesion, were unchanged after the training. However, training modified distribution of BDNF in the processes with its predominance in the longer and thicker ones. It also caused selective up-regulation of BDNF in two classes of cells (soma ranging between 100-400 um2 and over 1000 um2) of the ventrolateral and laterodorsal motor nuclei. Conclusions: Our results show that it is not BDNF deficit that determines lack of functional improvement in spinal animals. They indicate selectivity of up-regulation of BDNF in distinct subpopulations of cells in the motor nuclei which leads to changes of innervation targeting motoneurons, tuned up by locomotor activity as indicated by a region-specific increase of presynaptic markers. http://www.biomedcentral.com/1471-2202/10/144 Matylda Macias Dorota Nowicka Artur Czupryn Dorota Sulejczak Malgorzata Skup Jolanta Skangiel-Kramska Julita Czarkowska-Bauch BMC Neuroscience 2009, 10:144 2009-12-04T00:00:00Z doi:10.1186/1471-2202-10-144 BMC Neuroscience 1471-2202 10 144 2009-12-04T00:00:00Z PDF Background: Due to auditory experience, musicians have better auditory expertise than non-musicians. An increased neocortical activity during auditory oddball stimulation was observed in different studies for musicians and for non-musicians after discrimination training. This suggests a modification of synaptic strength among simultaneously active neurons due to the training. We used amplitude-modulated tones (AM) presented in an oddball sequence and manipulated their carrier or modulation frequencies. We investigated non-musicians in order to see if behavioral discrimination training could modify the neocortical activity generated by change detection of AM tone attributes (carrier or modulation frequency). Cortical evoked responses like N1 and mismatch negativity (MMN) triggered by sound changes were recorded by a whole head magnetoencephalographic system (MEG). We investigated (i) how the auditory cortex reacts to pitch difference (in carrier frequency) and changes in temporal features (modulation frequency) of AM tones and (ii) how discrimination training modulates the neuronal activity reflecting the transient auditory responses generated in the auditory cortex. Results: The results showed that, additionally to an improvement of the behavioral discrimination performance, discrimination training of carrier frequency changes significantly modulates the MMN and N1 response amplitudes after the training. This process was accompanied by an attention switch to the deviant stimulus after the training procedure identified by the occurrence of a P3a component. In contrast, the training in discrimination of modulation frequency was not sufficient to improve the behavioral discrimination performance and to alternate the cortical response (MMN) to the modulation frequency change. The N1 amplitude, however, showed significant increase after and one week after the training. Similar to the training in carrier frequency discrimination, a long lasting involuntary attention to the deviant stimulus was observed. Conclusions: We found that discrimination training differentially modulates the cortical responses to pitch changes and to envelope fluctuation changes of AM tones. This suggests that discrimination between AM tones requires additional neuronal mechanisms compared to discrimination process between pure tones. After the training, the subjects demonstrated an involuntary attention switch to the deviant stimulus (represented by the P3a-component in the MEG) even though attention was not prerequisite. http://www.biomedcentral.com/1471-2202/10/143 Rossitza Draganova Andreas Wollbrink Matthias Schulz Hidehiko Okamoto Christo Pantev BMC Neuroscience 2009, 10:143 2009-12-01T00:00:00Z doi:10.1186/1471-2202-10-143 BMC Neuroscience 1471-2202 10 143 2009-12-01T00:00:00Z PDF Background: Spinal Muscular Atrophy (SMA) is the leading genetic cause of infantile death. It is caused by the loss of functional Survival Motor Neuron 1 (SMN1). There is a nearly identical copy gene, SMN2, but it is unable to rescue from disease due to an alternative splicing event that excises a necessary exon (exon 7) from the majority of SMN2-derived transcripts. While SMN-delta7 protein has severely reduced functionality, the exon 7 sequences may not be specifically required for all activities. Therefore, aminoglycoside antibiotics previously shown to suppress stop codon recognition and promote translation read-through have been examined to increase the length of the SMN-delta7 C-terminus. Results: Here we demonstrate that subcutaneous-administration of a read-through inducing compound (TC007) to an intermediate SMA model (Smn-/-; SMN2+/+; SMN-delta7) had beneficial effects on muscle fiber size and gross motor function. Conclusions: Delivery of the read-through inducing compound TC007 reduces the disease-associated phenotype in SMA mice, however, does not significantly extend survival. http://www.biomedcentral.com/1471-2202/10/142 Virginia Mattis Marina Fosso Cheng-Wei Chang Christian Lorson BMC Neuroscience 2009, 10:142 2009-11-30T00:00:00Z doi:10.1186/1471-2202-10-142 BMC Neuroscience 1471-2202 10 142 2009-11-30T00:00:00Z PDF Background: Changes in neuronal excitability, synaptic efficacy and generally in cell signaling often result from insertion of key molecules into plasma membrane (PM). Many of the techniques used for monitoring PM insertion lack either spatial or temporal resolution. Results: We improved the imaging method based on time-lapse total internal reflection fluorescence (TIRF) microscopy and pHluorin tagging by supplementing it with a repetitive extracellular acidification protocol. We illustrate the applicability of this method by showing that brief activation of NMDA receptors ("chemical LTP") in cultured hippocampal neurons induced a persistent PM insertion of glutamate receptors containing the pHluorin-tagged GluR-A(flip) subunits. Conclusions: The repetitive acidification technique provides a more accurate way of monitoring the PM-inserted fraction of fluorescently tagged molecules and offers a good temporal and spatial resolution. http://www.biomedcentral.com/1471-2202/10/141 Serguei Khiroug Evgeny Pryazhnikov Sarah Coleman Andreas Jeromin Kari Keinanen Leonard Khiroug BMC Neuroscience 2009, 10:141 2009-11-30T00:00:00Z doi:10.1186/1471-2202-10-141 BMC Neuroscience 1471-2202 10 141 2009-11-30T00:00:00Z PDF Background: The shading of an object provides an important cue for recognition, especially for determining its 3D shape. However, neuronal mechanisms that allow the recovery of 3D shape from shading are poorly understood. The aim of our study was to determine the neuronal basis of 3D shape from shading coding in area V4 of the awake macaque monkey. Results: We recorded the responses of V4 cells to stimuli presented parafoveally while the monkeys fixated a central spot. We used a set of stimuli made of 8 different 3D shapes illuminated from 4 directions (from above, the left, the right and below) and different 2D controls for each stimulus. The results show that V4 neurons present a broad selectivity to 3D shape and illumination direction, but without a preference for a unique illumination direction. However, 3D shape and illumination direction selectivities are correlated suggesting that V4 neurons can use the direction of illumination present in complex patterns of shading present on the surface of objects. In addition, a vast majority of V4 neurons (78%) have statistically different responses to the 3D and 2D versions of the stimuli, while responses to 3D are not systematically stronger than those to 2D controls. However, a hierarchical cluster analysis showed that the different classes of stimuli (3D, 2D controls) are clustered in the V4 cells response space suggesting a coding of 3D stimuli based on the population response. The different illumination directions also tend to be clustered in this space. Conclusion: Together, these results show that area V4 participates, at the population level, in the coding of complex shape from the shading patterns coming from the illumination of the surface of corrugated objects. Hence V4 provides important information for one of the steps of cortical processing of the 3D aspect of objects in natural light environment. http://www.biomedcentral.com/1471-2202/10/140 Fabrice Arcizet Christophe Jouffrais Pascal Girard BMC Neuroscience 2009, 10:140 2009-11-30T00:00:00Z doi:10.1186/1471-2202-10-140 BMC Neuroscience 1471-2202 10 140 2009-11-30T00:00:00Z PDF Background: : Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. However, Molecular mechanisms that regulate neuronal cell proliferation in the dentate gyrus (DG) following ischemic stroke insult are poorly understood. This study was designed to investigate the potential regulatory capacity of non-receptor tyrosine kinase Src on ischemia-stimulated cell proliferation in the adult DG and its underlying mechanism. Results: : Src kinase activated continuously in the DG 24 h and 72h after transient global ischemia, while SU6656, the Src kinase inhibitor significantly decreased the number of bromodeoxyuridine (BrdU) labeling-positive cells of rats 7 days after cerebral ischemia in the DG, as well as down-regulated Raf phosphorylation at Tyr(340/341) site, and its down-stream signaling molecules ERK and CREB expression followed by 24 h and 72h of reperfusion, suggesting a role of Src kinase as an enhancer on neuronal cell proliferation in the DG via modifying the Raf/ERK/CREB cascade. This hypothesis is supported by further findings that U0126, the ERK inhibitor, induced a reduction of adult hippocampal progenitor cells in DG after cerebral ischemia and down-regulated phospho-ERK and phospho-CREB expression, but no effect was detected on the activities of Src and Raf.CONCLUSION: Src kinase increase numbers of newborn neuronal cells in the DG via the activation of Raf/ERK/CREB signaling cascade after cerebral ischemia. http://www.biomedcentral.com/1471-2202/10/139 He-Ping Tian Bao-Sheng Huang Jie Zhao Xiao-Han Hu Jun Guo Li-Xin Li BMC Neuroscience 2009, 10:139 2009-11-27T00:00:00Z doi:10.1186/1471-2202-10-139 BMC Neuroscience 1471-2202 10 139 2009-11-27T00:00:00Z PDF Background: In this paper we explored thalamocortical functional connectivity in a group of eight patients suffering from peripheral neuropathic pain (diabetic pain), and compared it with that of a group of healthy subjects. We hypothesized that functional interconnections between the thalamus and cortex can be altered after years of ongoing chronic neuropathic pain. Results: Functional connectivity was studied through a resting state functional magnetic resonance imaging (fMRI) paradigm: temporal correlations between predefined regions of interest (primary somatosensory cortex, ventral posterior lateral thalamic nucleus, medial dorsal thalamic nucleus) and the rest of the brain were systematically investigated. The patient group showed decreased resting state functional connectivity between the thalamus and the cortex. Conclusion: This supports the idea that chronic pain can alter thalamocortical connections causing a disruption of thalamic feedback, and the view of chronic pain as a thalamocortical dysrhythmia. http://www.biomedcentral.com/1471-2202/10/138 Franco Cauda Katiuscia Sacco Federico D'Agata Sergio Duca Dario Cocito Giuliano Geminiani Filippo Migliorati Gianluca Isoardo BMC Neuroscience 2009, 10:138 2009-11-26T00:00:00Z doi:10.1186/1471-2202-10-138 BMC Neuroscience 1471-2202 10 138 2009-11-26T00:00:00Z XML Background: In the absence of overt stimuli, the brain shows correlated fluctuations in functionally related brain regions. Approximately ten largely independent resting state networks (RSNs) showing this behaviour have been documented to date. Recent studies have reported the existence of an RSN in the basal ganglia - albeit inconsistently and without the means to interpret its function. Using two large study groups with different resting state conditions and MR protocols, the reproducibility of the network across subjects, behavioural conditions and acquisition parameters is assessed. Independent Component Analysis (ICA), combined with novel analyses of temporal features, is applied to establish the basis of signal fluctuations in the network and its relation to other RSNs. Reference to prior probabilistic diffusion tractography work is used to identify the basal ganglia circuit to which these fluctuations correspond. Results: An RSN is identified in the basal ganglia and thalamus, comprising the pallidum, putamen, subthalamic nucleus and substantia nigra, with a projection also to the supplementary motor area. Participating nuclei and thalamo-cortical connection probabilities allow this network to be identified as the motor control circuit of the basal ganglia. The network was reproducibly identified across subjects, behavioural conditions (fixation, eyes closed), field strength and echo-planar imaging parameters. It shows a frequency peak at 0.025 ± 0.007 Hz and is most similar in spectral composition to the Default Mode (DM), a network of regions that is more active at rest than during task processing. Frequency features allow the network to be classified as an RSN rather than a physiological artefact. Fluctuations in this RSN are correlated with those in the task-positive fronto-parietal network and anticorrelated with those in the DM, whose hemodynamic response it anticipates. Conclusion: Although the basal ganglia RSN has not been reported in most ICA-based studies using a similar methodology, we demonstrate that it is reproducible across subjects, common resting state conditions and imaging parameters, and show that it corresponds with the motor control circuit. This characterisation of the basal ganglia network opens a potential means to investigate the motor-related neuropathologies in which the basal ganglia are involved. http://www.biomedcentral.com/1471-2202/10/137 Simon Robinson Gianpaolo Basso Nicola Soldati Uta Sailer Jorge Jovicich Lorenzo Bruzzone Ilse Kryspin-Exner Herbert Bauer Ewald Moser BMC Neuroscience 2009, 10:137 2009-11-23T00:00:00Z doi:10.1186/1471-2202-10-137 BMC Neuroscience 1471-2202 10 137 2009-11-23T00:00:00Z XML Background: Repeated rehearsal is one method by which verbal material may be transferred from short- to long-term memory. We hypothesised that extended engagement of memory structures through prolonged rehearsal would result in enhanced efficacy of recall and also of brain structures implicated in new learning. Twenty-four normal participants aged 55-70 (mean = 60.1) engaged in six weeks of rote learning, during which they learned 500 words per week every week (prose, poetry etc.). An extensive battery of memory tests was administered on three occasions, each six weeks apart. In addition, proton magnetic resonance spectroscopy (1H-MRS) was used to measure metabolite levels in seven voxels of interest (VOIs) (including hippocampus) before and after learning. Results: Results indicate a facilitation of new learning that was evident six weeks after rote learning ceased. This facilitation occurred for verbal/episodic material only, and was mirrored by a metabolic change in left posterior hippocampus, specifically an increase in NAA/(Cr+Cho) ratio. Conclusion: Results suggest that repeated activation of memory structures facilitates anamnesis and may promote neuronal plasticity in the ageing brain, and that compliance is a key factor in such facilitation as the effect was confined to those who engaged fully with the training. http://www.biomedcentral.com/1471-2202/10/136 Richard Roche Sinead Mullally Jonathan McNulty Judy Hayden Paul Brennan Colin Doherty Mary Fitzsimons Deirdre McMackin Julie Prendergast Sunita Sukumaran Maeve Mangaoang Ian Robertson Shane O'Mara BMC Neuroscience 2009, 10:136 2009-11-20T00:00:00Z doi:10.1186/1471-2202-10-136 BMC Neuroscience 1471-2202 10 136 2009-11-20T00:00:00Z XML Background: Chronic systemic inflammation triggers alterations in the central nervous system that may relate to the underlying inflammatory component reported in neurodegenerative disorders such as multiple sclerosis and Alzheimer's disease. However, it is far from being understood whether and how peripheral inflammation contributes to induce brain inflammatory response in such illnesses. As part of the barriers that separate the blood from the brain, the choroid plexus conveys inflammatory immune signals into the brain, largely through alterations in the composition of the cerebrospinal fluid. Results: In the present study we investigated the mouse choroid plexus gene expression profile, using microarray analyses, in response to a repeated inflammatory stimulus induced by the intraperitoneal administration of lipopolysaccharide every two weeks for a period of three months; mice were sacrificed 3 and 15 days after the last lipopolysaccharide injection. The data show that the choroid plexus displays a sustained response to the repeated inflammatory stimuli by altering the expression profile of several genes. From a total of 24,000 probes, 369 are up-regulated and 167 are down-regulated 3 days after the last lipopolysaccharide injection, while at 15 days the number decreases to 98 and 128, respectively. The pathways displaying the most significant changes include those facilitating entry of cells into the cerebrospinal fluid, and those participating in the innate immune response to infection. Conclusion: These observations contribute to a better understanding of the brain response to peripheral inflammation and pave the way to study their impact on the progression of several disorders of the central nervous system in which inflammation is known to be implicated. http://www.biomedcentral.com/1471-2202/10/135 Fernanda Marques Joao Sousa Giovanni Coppola Daniel Geschwind Nuno Sousa Joana Palha Margarida Correia-Neves BMC Neuroscience 2009, 10:135 2009-11-18T00:00:00Z doi:10.1186/1471-2202-10-135 BMC Neuroscience 1471-2202 10 135 2009-11-18T00:00:00Z XML