bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of S100B on local field potential patterns in anesthetized and kainic acid‐induced seizure conditions in vivo
Authors: Sakatani Seiichi , Seto‐Ohshima Akiko , Itohara Shigeyoshi , Hirase Hajime 
Published: February 2007

AbstractS100B is a calcium‐binding protein predominantly expressed in astrocytes. Previous studies using gene‐manipulated animals have suggested that the protein has a role in synaptic plasticity and learning. In order to assess the physiological roles of the protein in active neural circuitry, we recorded spontaneous neural activities from various layers of the neocortex and hippocampus in urethane‐anesthetized S100B knockout (KO) and wildtype (WT) control mice. Typical local field oscillation patterns including the slow (0.5–2 Hz) oscillations in the neocortex, theta (3–8 Hz) and sharp wave‐associated ripple (120–180 Hz) oscillations in the hippocampus were observed in both genotypes. Comparisons of the frequency, power and peak amplitude have shown that these oscillatory patterns were virtually indistinguishable between WT and KO. When seizure was induced by intraperitoneal injection of kainic acid, a difference between WT and KO appeared in the CA1 radiatum local field potential pattern, where seizure events were characterized by prominent appearance of hyper‐synchronous gamma band (30–80 Hz) activity. Although both genotypes developed seizures within 40 min, the gamma amplitude was significantly smaller during the development of seizures in KO mice. Our results suggest that deficiency of S100B does not have a profound impact on spontaneous neural activity in normal conditions. However, when neural activity was sufficiently raised, activation of S100B‐related pathways may take effect, resulting in modulation of neural activities.
MAPKs are key players in mediating cytokine release and cell death induced by unconjugated bilirubin in cultured rat cortical astrocytes
Authors: Fernandes Adelaide , Falcão Ana S. , Silva Rui F. M. , Brito Maria A. , Brites Dora 
Published: February 2007

AbstractWhen activated by unconjugated bilirubin (UCB), astrocytes are important sources of inflammatory mediators such as TNF‐α, IL‐1β and IL‐6, which may contribute for the neurotoxicity observed during severe neonatal hyperbilirubinemia. In the present study, we have addressed the role of the mitogen‐activated protein kinases (MAPKs) p38, Jun N‐terminal kinase (JNK)1/2 and extracellular signal‐regulated kinase (ERK)1/2 pathways and their relation with the nuclear factor κB (NF‐κB) cascade in the signalling events involved in cytokine release and cell death caused by UCB in primary cultures of rat astrocytes. Stimulation of astrocytes with UCB in the presence of all the MAPK inhibitors prevented UCB‐induced release of TNF‐α and IL‐6, while IL‐1β secretion was only reduced by JNK1/2 and ERK1/2 inhibitors. In addition, activation of the NF‐κB transcription factor, needed for cytokine release by UCB‐stimulated astrocytes, was shown to be dependent on JNK1/2 and ERK1/2 phosphorylation. Moreover, all MAPK inhibitors prevented astroglial apoptosis triggered by UCB. Interestingly, UCB‐induced lactate dehydrogenase release was prevented by blockade of JNK1/2, ERK1/2 and NF‐κB cascades but enhanced by p38 inhibition. Taken together, our data demonstrate for the first time that MAPK transduction pathways are key players in the UCB‐induced inflammatory response and cell death in astrocytes, probably also involving NF‐κB modulation. These findings contribute to unraveling the complex mechanisms of astrocyte reactivity to UCB and may ultimately prove useful in the development of new therapeutic strategies to prevent nerve cell damage during acute bilirubin encephalopathy.
Axonal accumulation of synaptic markers in APP transgenic Drosophila depends on the NPTY motif and is paralleled by defects in synaptic plasticity
Authors: Rusu Patricia , Jansen Anna , Soba Peter , Kirsch Joachim , Löwer Alexander , Merdes Gunter , Kuan Yung‐Hui , Jung Anita , Beyreuther Konrad , Kjaerulff Ole , Kins Stefan 
Published: February 2007

AbstractAlzheimer's disease (AD) is characterized by neurofibrillary tangles and extracellular plaques, which consist mainly of β‐amyloid derived from the β‐amyloid precursor protein (APP). An additional feature of AD is axonopathy, which might contribute to impairment of cognitive functions. Specifically, axonal transport defects have been reported in AD animal models, including mice and flies that overexpress APP and tau. Here we demonstrate that the APP‐induced traffic jam of vesicles in peripheral nerves of Drosophila melanogaster larvae depends on the four residues NPTY motif in the APP intracellular domain. Furthermore, heterologous expression of Fe65 and JIP1b, scaffolding proteins interacting with the NPTY motif, also perturb axonal transport. Together, these data indicate that JIP1b or Fe65 may be involved in the APP‐induced axonal transport defect. Moreover, we have characterized neurotransmission at the neuromuscular junction in transgenic larvae that express human APP. Consistent with the observation that these larvae do not show any obvious movement deficits, we found no changes in basal synaptic transmission. However, short‐term synaptic plasticity was affected by overexpression of APP. Together, our results show that overexpression of APP induces partial stalling of axonal transport vesicles, paralleled by abnormalities in synaptic plasticity, which may provide a functional link to the deterioration of cognitive functions observed in AD.
Lateralized activation of Cluster N in the brains of migratory songbirds
Authors: Liedvogel Miriam , Feenders Gesa , Wada Kazuhiro , Troje Nikolaus F. , Jarvis Erich D. , Mouritsen Henrik 
Published: February 2007

AbstractCluster N is a cluster of forebrain regions found in night‐migratory songbirds that shows high activation of activity‐dependent gene expression during night‐time vision. We have suggested that Cluster N may function as a specialized night‐vision area in night‐migratory birds and that it may be involved in processing light‐mediated magnetic compass information. Here, we investigated these ideas. We found a significant lateralized dominance of Cluster N activation in the right hemisphere of European robins (Erithacus rubecula). Activation predominantly originated from the contralateral (left) eye. Garden warblers (Sylvia borin) tested under different magnetic field conditions and under monochromatic red light did not show significant differences in Cluster N activation. In the fairly sedentary Sardinian warbler (Sylvia melanocephala), which belongs to the same phyolgenetic clade, Cluster N showed prominent activation levels, similar to that observed in garden warblers and European robins. Thus, it seems that Cluster N activation occurs at night in all species within predominantly migratory groups of birds, probably because such birds have the capability of switching between migratory and sedentary life styles. The activation studies suggest that although Cluster N is lateralized, as is the dependence on magnetic compass orientation, either Cluster N is not involved in magnetic processing or the magnetic modulations of the primary visual signal, forming the basis for the currently supported light‐dependent magnetic compass mechanism, are relatively small such that activity‐dependent gene expression changes are not sensitive enough to pick them up.
A novel neurotransmitter‐independent communication pathway between axons and glial cells
Authors: Hartl Sandra , Heil Jan E. , Hirsekorn Andrea , Lohr Christian 
Published: February 2007

AbstractRecent studies have provided evidence that transmitters released by neurons can activate glial receptors and stimulate calcium signalling in glial cells. Glial calcium signalling, in turn, may affect neuronal performance such as long‐term changes in synaptic efficacy. Olfactory ensheathing cells (OECs) are a special glial cell type in vertebrates and insects and promote axon growth in the developing and mature nervous system. Physiological properties of OECs, however, have not been studied so far in detail. We measured changes in the calcium concentration in OECs of the moth Manduca sexta, in situ and in vivo. Electrical stimulation of olfactory receptor neurons in pupae or odour stimulation of receptor neurons in adults resulted in calcium transients in OECs. Olfactory receptor axons release acetylcholine; however, application of acetylcholine or other transmitters such as glutamate, GABA or nitric oxide did not induce calcium transients in OECs. Upon nerve stimulation, extracellular potassium rose by several millimolar as measured with potassium‐sensitive microelectrodes. When potassium in the perfusion saline was increased from 4 to 10 mm or higher, voltage‐dependent calcium transients in OECs that resembled stimulation‐induced calcium transients were evoked. Blocking neuronal potassium channels with TEA reduced both the stimulation‐induced increases in extracellular potassium and the calcium transients in OECs, whereas calcium transients in receptor axons were augmented. Our results show for the first time that accumulation of potassium, released by electrically active axons, is sufficient to evoke voltage‐dependent calcium influx into glial cells, whereas neurotransmitters appear not to be involved in this neuron–glia communication in Manduca.
Changes in activity of the striatum during formation of a motor habit
Authors: Tang Chengke , Pawlak Anthony P. , Prokopenko Volodymyr , West Mark O. 
Published: February 2007

AbstractTo examine experience‐dependent plasticity of striatal neurons during habit learning in awake, freely moving animals, single neurons in the dorsolateral striatum (54 neurons related specifically to vertical head movement and 14 unresponsive neurons, i.e. not related to any body movement) were recorded and tracked off‐line to assess changes in firing rate over sessions as performance of instrumental head movement became automatic and habitual. Rats were trained to emit operant vertical head movements that triggered water delivery for 14 sessions (2 h per session, one session per day). Rats significantly increased the number and efficiency of head movements over sessions until reaching asymptotic behaviour. Habit formation was indicated by significantly higher levels of instrumental responding exhibited by rats during a late, relative to an early, session in which the reward was devalued. As head movements became habitual across sessions, most head movement‐related neurons (89%) exhibited decreased firing rate, while a small population (11%) exhibited increased or maintained firing rate. The rate of decrease in firing by the majority correlated with the rate of improvement in movement efficiency over sessions. All unresponsive neurons, though not apparently related to movement, exhibited decreased firing rate over sessions. Our findings suggest that, during habit learning, the striatum may shift from facilitating acquisition of efficient movement with a large population of neurons to modulating or maintaining habitual movement with stronger firing of fewer movement‐related neurons.
The involvement of primary motor cortex in mental rotation revealed by transcranial magnetic stimulation
Authors: Eisenegger C. , Herwig U. , Jäncke L. 
Published: February 2007

AbstractWe used single‐pulse transcranial magnetic stimulation of the left primary hand motor cortex and motor evoked potentials of the contralateral right abductor pollicis brevis to probe motor cortex excitability during a standard mental rotation task. Based on previous findings we tested the following hypotheses. (i) Is the hand motor cortex activated more strongly during mental rotation than during reading aloud or reading silently? The latter tasks have been shown to increase motor cortex excitability substantially in recent studies. (ii) Is the recruitment of the motor cortex for mental rotation specific for the judgement of rotated but not for nonrotated Shepard & Metzler figures? Surprisingly, motor cortex activation was higher during mental rotation than during verbal tasks. Moreover, we found strong motor cortex excitability during the mental rotation task but significantly weaker excitability during judgements of nonrotated figures. Hence, this study shows that the primary hand motor area is generally involved in mental rotation processes. These findings are discussed in the context of current theories of mental rotation, and a likely mechanism for the global excitability increase in the primary motor cortex during mental rotation is proposed.
Regulation of the subthreshold chloride conductance in the rat sympathetic neuron
Authors: Sacchi Oscar , Rossi Maria Lisa , Canella Rita , Fesce Riccardo 
Published: February 2007

AbstractThe mechanisms that control chloride conductance (gCl) in the rat sympathetic neuron have been studied by the two‐electrode voltage‐clamp technique in mature, intact superior cervical ganglia in vitro. In addition to voltage dependence in the membrane potential range −120/−50 mV, gCl displays time‐ and activity‐dependent regulation (sensitization). The resting membrane potential is governed by voltage‐dependent gK and gCl, which determine values of cell input conductance ranging from 7 to 18 nS (full deactivation) to an upper value of about 130 nS (full activation and maximal gCl sensitization). The quiescent neuron, held at constant membrane potential, spontaneously and gradually moved from a low‐ to a high‐conductance status. An increase (about 40 nS) in gCl accounted for this phenomenon, which could be prevented by imposing intermittent hyperpolarizing episodes. Following spike firing, gCl increased by 20–33 nS, independent of the cell conductance value preceding tetanization, and thereafter decayed to the pre‐stimulus level within 5 min. Intracellular sodium depletion and its successive ionophoretic restoration moved the neuron from a stable low‐conductance state to maximum gCl sensitization, pointing to a link between gCl sensitization and [Na+]i. The dependence of gCl build‐up on [Na+]i and the time‐course of such Na+‐related modulation have been examined: gCl sensitization was absent at 0 [Na+]i, was well developed (20 nS) at 15 mm and tended towards a saturating value of 60 nS for higher [Na+]i. Sensitization was transient in response to neuron activity. In the silent neuron, sensitization of gCl shifted membrane potential over a range of about 15 mV.
High‐frequency stimulation of the subthalamic nucleus modulates the activity of pedunculopontine neurons through direct activation of excitatory fibres as well as through indirect activation of inhibitory pallidal fibres in the rat
Authors: Florio Tiziana , Scarnati Eugenio , Confalone Giuseppina , Minchella Daniela , Galati Salvatore , Stanzione Paolo , Stefani Alessandro , Mazzone Paolo 
Published: February 2007

AbstractRecent data suggest a potential role of pedunculopontine nucleus (PPN) electrical stimulation in improving gait and posture in Parkinson's disease. Because the PPN receives fibres from the subthalamic nucleus (STN), we investigated the effects of STN‐high‐frequency stimulation (HFS) on PPN neuronal activity in intact rats and in rats bearing either an ibotenate lesion of the entopeduncular nucleus (EP) or a lesion of the substantia nigra (SN). The main response of PPN neurons to STN single‐shock stimulations in the three experimental groups was a short latency (4.5 ± 2.1 ms) and brief (15.3 ± 6.5 ms) excitation. This response was maintained during 1–5 s of STN‐HFS (130 Hz, 60 µs, 100–1000 µA). In EP‐lesioned rats the percentage (75.0%) of PPN neurons showing a modulation of activity following STN‐HFS was significantly higher compared with that observed in intact (39.7%) and in SN‐lesioned rats (35.4%). Furthermore, in EP‐lesioned rats the most frequent response of PPN neurons following STN‐HFS was a 5–20 s excitation, which was present in 76.6% of responsive neurons in comparison to 15.4% and 9.1% of neurons responsive in intact and in 6‐hydroxydopamine‐lesioned rats, respectively. Neurons responsive to STN‐HFS in the three experimental groups showed either a sharp positively skewed distribution of interspike intervals or multisecond oscillations in autocorrelograms. The results support that STN‐HFS modulates the PPN through a balance of excitatory and inhibitory influences, which may be independent from the dopaminergic nigral neurons. In the absence of inhibitory EP fibres, the direct excitatory influence exerted by the STN on the PPN appears to predominate.
Characterization of a transneuronal cytokine family Cbln − regulation of secretion by heteromeric assembly
Authors: Iijima Takatoshi , Miura Eriko , Matsuda Keiko , Kamekawa Yuichi , Watanabe Masahiko , Yuzaki Michisuke 
Published: February 2007

AbstractCbln1, a member of the C1q and tumor necrosis factor superfamily, plays crucial roles as a cerebellar granule cell‐derived transneuronal regulator of synapse integrity and plasticity in Purkinje cells. Although other Cbln family members, Cbln2–Cbln4, have distinct spatial and temporal patterns of expression throughout the CNS, their biochemical and biological properties have remained largely uncharacterized. Here, we demonstrated that in mammalian heterologous cells, Cbln2 and Cbln4 were secreted as N‐linked glycoproteins, like Cbln1. In contrast, despite the presence of a functional signal sequence, Cbln3 was not secreted when expressed alone but was retained in the endoplasmic reticulum (ER) or cis‐Golgi because of its N‐terminal domain. All members of the Cbln family formed not only homomeric but also heteromeric complexes with each other in vitro. Accordingly, when Cbln1 and Cbln3 were co‐expressed in heterologous cells, a proportion of the Cbln1 proteins was retained in the ER or cis‐Golgi; conversely, some Cbln3 proteins were secreted together with Cbln1. Similarly, in wild‐type granule cells expressing Cbln1 and Cbln3, Cbln3 proteins were partially secreted and reached postsynaptic sites on Purkinje cell dendrites, while Cbln3 was almost completely degraded in cbln1‐null granule cells. These results indicate that like Cbln1, Cbln2 and Cbln4 may also serve as transneuronal regulators of synaptic functions in various brain regions. Furthermore, heteromer formation between Cbln1 and Cbln3 in cerebellar granule cells may modulate each other's trafficking and signaling pathways; similarly, heteromerization of other Cbln family proteins may also have biological significance in other neurons.
Differential cortical activity for precision and whole‐hand visually guided grasping in humans
Authors: Begliomini Chiara , Wall Matthew B. , Smith Andrew T. , Castiello Umberto 
Published: February 2007

AbstractEffective grasping involves the remarkable ability to implement multiple grasp configurations such as precision grip (PG; opposition between the index finger and thumb) and whole‐hand grasp (WHG), depending on the properties of the object grasped (e.g. size, shape and weight). In the monkey brain, different groups of cells in the anterior–lateral bank of the intraparietal sulcus (area AIP) are differentially active for various hand configurations during grasping of differently shaped objects. Visually guided grasping studies in humans suggest the anterior intraparietal sulcus (aIPS) as the homologue of macaque area AIP, but leave unresolved the question of whether activity in human aIPS reflects the relationship between object size and grasp configuration, as in macaques. To address this issue, a human fMRI study was conducted in which objects were grasped with the right hand while object size was varied. The results indicated that the left aIPS was active when the subjects naturally adopted a PG to grasp the small object but showed a much weaker response when subjects naturally adopted a WHG to grasp the large object. The primary motor cortex and somatosensory cortices were active for both PG and WHG. Our results suggest that, in humans, the aIPS is centrally involved in determining the type of grasp.
Identification of self‐replicating multipotent progenitors in the embryonic nervous system by high Notch activity and Hes5 expression
Authors: Basak Onur , Taylor Verdon 
Published: February 2007

AbstractDiscrimination of neural stem cells from other progenitors in the developing mammalian brain has been hampered by the lack of specific markers. Identifying the progenitor pools and signalling pathways that guide mammalian neurogenesis are central to understanding the complex mechanisms that govern development of the nervous system. Notch signalling plays a pivotal role in the development of the mammalian nervous system by maintaining multipotent neural stem cells and regulating their fate. In order to identify putative neural stem cells in situ, we generated transgenic mice that express Green Fluorescent Protein (GFP) and report Notch signalling activity in the developing CNS. Here we show the subdivision of progenitors within the neural tube of these mice. We purify progenitors from the neural tube and show that cells with the highest levels of Notch‐reporter activity have self‐renewal capability and multipotency, whereas those lacking Hes5 expression do not form neurospheres in vitro. Using marker protein co‐expression and cell sorting, we show that both neuroepithelial cells as well as some radial glia at all axial levels of the embryonic neural tube display active Notch signalling. However, Tbr2‐positive basal progenitors of the developing telencephalon and differentiating Islet1/2‐ and Lim1‐positive motor neurons outside the ventricular zone do not express Hes5‐GFP. Quantitative analysis showed that Hes5 expression correlates better with neural stem cell potential than expression of the related gene Hes1. Thus, Notch activity through Hes5 identifies multipotent progenitors with stem cell properties and subdivides the different progenitors into defined pools.
Bilateral high‐frequency stimulation of the subthalamic nucleus on attentional performance: transient deleterious effects and enhanced motivation in both intact and parkinsonian rats
Authors: Baunez Christelle , Christakou Anastasia , Chudasama Yogita , Forni Claude , Robbins Trevor W. 
Published: February 2007

AbstractIt is now well established that subthalamic nucleus high‐frequency stimulation (STN HFS) alleviates motor problems in Parkinson's disease. However, its efficacy for cognitive function remains a matter of debate. The aim of this study was to assess the effects of STN HFS in rats performing a visual attentional task. Bilateral STN HFS was applied in intact and in bilaterally dopamine (DA)‐depleted rats. In all animals, STN HFS had a transient debilitating effect on all the variables measured in the task. In DA‐depleted rats, STN HFS did not alleviate the deficits induced by the DA lesion such as omissions and latency to make correct responses, but induced perseverative approaches to the food magazine, an indicator of enhanced motivation. In sham‐operated controls, STN HFS significantly reduced accuracy and induced perseverative behaviour, mimicking partially the effects of bilateral STN lesions in the same task. These results are in line with the hypothesis that STN HFS only partially mimics inactivation of STN produced by lesioning and confirm the motivational exacerbation induced by STN inactivation.