bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cortical mechanisms of attention in time: neural correlates of the Lag‐1‐sparing phenomenon
Authors: Kessler Klaus , Schmitz Frank , Gross Joachim , Hommel Bernhard , Shapiro Kimron , Schnitzler Alfons 
Published: May 2005

AbstractIf humans monitor streams of rapidly presented (≈ 100‐ms intervals) visual stimuli, which are typically specific single letters of the alphabet, for two targets (T1 and T2), they often miss T2 if it follows T1 within an interval of 200–500 ms. If T2 follows T1 directly (within 100 ms; described as occurring at ‘Lag 1’), however, performance is often excellent: the so‐called ‘Lag‐1 sparing’ phenomenon. Lag‐1 sparing might result from the integration of the two targets into the same ‘event representation’, which fits with the observation that sparing is often accompanied by a loss of T1–T2 order information. Alternatively, this might point to competition between the two targets (implying a trade‐off between performance on T1 and T2) and Lag‐1 sparing might solely emerge from conditional data analysis (i.e. T2 performance given T1 correct). We investigated the neural correlates of Lag‐1 sparing by carrying out magnetoencephalography (MEG) recordings during an attentional blink (AB) task, by presenting two targets with a temporal lag of either 1 or 2 and, in the case of Lag 2, with a nontarget or a blank intervening between T1 and T2. In contrast to Lag 2, where two distinct neural responses were observed, at Lag 1 the two targets produced one common neural response in the left temporo‐parieto‐frontal (TPF) area but not in the right TPF or prefrontal areas. We discuss the implications of this result with respect to competition and integration hypotheses, and with respect to the different functional roles of the cortical areas considered. We suggest that more than one target can be identified in parallel in left TPF, at least in the absence of intervening nontarget information (i.e. masks), yet identified targets are processed and consolidated as two separate events by other cortical areas (right TPF and PFC, respectively).
Effects of LAR and PTP‐BL phosphatase deficiency on adult mouse retinal cells activated by lens injury
Authors: Lorber Barbara , Hendriks Wiljan J. A. J. , Van der Zee Catharina E. E. M. , Berry Martin , Logan Ann 
Published: May 2005

AbstractUsing intact and lens‐lesioned wildtype, leucocyte common antigen‐related phosphatase deficient (LARΔP) and protein tyrosine phosphatase (PTP)‐BAS‐like phosphatase deficient (PTP‐BLΔP) mice, we have evaluated the role of LAR and PTP‐BL in retinal ganglion cell survival and neuritogenesis, and survival of activated retinal glia in vitro. There were no differences in in vitro retinal ganglion cell neuritogenesis and survival, as well as in activated retinal glia survival between intact wildtype and intact LARΔP or PTP‐BLΔP mutant mice. In wildtype, LARΔP, and PTP‐BLΔP retinal cultures, pre‐conditioning by lens injury significantly increased retinal ganglion cell neuritogenesis and activated retinal glia numbers. However, in retinal cultures from lens‐lesioned LARΔP and PTP‐BLΔP mice, significantly smaller percentages of retinal ganglion cells grew neurites compared to lens‐lesioned wildtype cultures. Significantly increased numbers of retinal ganglion cells survived in retinal cultures from lens‐lesioned LARΔP mice compared to lens‐lesioned wildtypes. PTP‐BL phosphatase deficiency did not affect retinal ganglion cell survival in retinal cultures from lens‐lesioned mice, though activated retinal glia numbers were significantly reduced in cultures from lens‐lesioned PTP‐BLΔP mice compared to lens‐lesioned wildtypes. In summary, a functional phenotype was found in LARΔP and PTP‐BLΔP mice, that was only obvious in lens lesion‐stimulated retinal cultures. These observations suggest that LAR enhances retinal ganglion cell neurite initiation whilst suppressing retinal ganglion cell survival, and that PTP‐BL facilitates both retinal ganglion cell neurite initiation and survival of activated retinal glia.
Multimodal early onset stimulation combined with enriched environment is associated with reduced CNS lesion volume and enhanced reversal of neuromotor dysfunction after traumatic brain injury in rats
Authors: Maegele Marc , Lippert‐Gruener Marcela , Ester‐Bode Thorsten , Garbe Janika , Bouillon Bertil , Neugebauer Edmund , Klug Norfrid , Lefering Rolf , Neiss Wolfram F. , Angelov Doychin N. 
Published: May 2005

AbstractThis study was designed to determine whether exposure to multimodal early onset stimulation (MEOS) combined with environmental enrichment (EE) after traumatic brain injury (TBI) would improve neurological recovery and to elucidate its morphological correlates. Male Sprague–Dawley rats were subjected to lateral fluid percussion (LFP) brain injury or to sham operation. After LFP, one‐third of the animals (injured and sham) were placed under conditions of standard housing (SH), one‐third were kept in EE only, and one‐third received EE + MEOS. Assessment of neuromotor function 24 h post‐injury using a standardized composite neuroscore test revealed an identical pattern of neurological impairment in all animals subjected to LFP. Neuromotor dysfunction in SH animals remained on a similar level throughout the experiment, while improvements were noted in both other groups 7 days post‐injury (dpi). On 15 dpi, reversal of neuromotor dysfunction was significantly better in EE + MEOS animals vs. SH‐ and EE‐only groups. In parallel, the comparison of lesion volume in EE + MEOS‐ vs. EE‐only vs. SH rats revealed that animals exposed to EE + MEOS had consistently the lowest values (mm3, mean ± SD; n = 6 rats in each group) as measured in serial brain sections immunostained for neuron‐specific enolase (5.2 ± 3.4 ≤ 5.5 ± 4.1 < 9.5 ± 1.9), caspase 3‐active/C3A (5.9 ± 4.0 ≤ 6.4 ± 3.9 < 10.3 ± 1.8) and glial fibrillary acidic protein (6.0 ± 3.4 ≤ 6.5 ± 4.3 < 10.7 ± 1.2). This first report on the effect of EE + MEOS treatment strongly indicates that the combined exposure reduces CNS scar formation and reverses neuromotor deficits after TBI in rats.
Pregnenolone sulphate attenuates AMPA cytotoxicity on rat cortical neurons
Authors: Shirakawa Hisashi , Katsuki Hiroshi , Kume Toshiaki , Kaneko Shuji , Akaike Akinori 
Published: May 2005

AbstractNeuroactive steroids can modulate brain excitability by interaction with several neurotransmitter receptor‐associated channels. These compounds may thus exert profound influences on excitotoxic injury, i.e. neuronal cell death triggered by over‐activation of glutamate receptors. It has been reported that pregnenolone sulphate (PS) and pregnenolone hemisuccinate (PHS) augment N‐methyl‐d‐aspartate (NMDA) neurotoxicity in rat cultured neurons. Here we show that the effects of neuroactive steroids on AMPA cytotoxicity display features distinct from those on NMDA cytotoxicity. Concomitant application of PS (30–300 µm) attenuated, rather than augmented, AMPA neurotoxicity in cortical slice cultures in a concentration‐dependent manner, whereas various other steroids including pregnenolone and PHS had no effect. Inhibition of steroid sulphatase by estrone‐3‐O‐sulphamate led to a shift of the minimum effective concentration of PS against AMPA cytotoxicity from 30 to 10 µm. The protective action of PS was not affected by inhibition of protein synthesis or by blockade of glucocorticoid receptors, GABAA receptors or σ‐receptors. In dissociated cortical neurons, PS attenuated AMPA‐induced inward currents whereas pregnenolone and PHS exhibited no significant effect. Thus, with strict structural specificity, PS but not pregnenolone or PHS attenuates AMPA cytotoxicity, probably by inhibiting activities of AMPA receptor‐associated channels.
Activation of the JNK–c‐Jun pathway during the early phase of neuronal apoptosis induced by PrP106–126 and prion infection
Authors: Carimalo J. , Cronier S. , Petit G. , Peyrin J.‐M , Boukhtouche F. , Arbez N. , Lemaigre‐Dubreuil Y. , Brugg B. , Miquel M.‐C 
Published: May 2005

AbstractPrion diseases are neurodegenerative pathologies characterized by apoptotic neuronal death. Although the late execution phase of neuronal apoptosis is beginning to be characterized, the sequence of events occurring during the early decision phase is not yet well known. In murine cortical neurons in primary culture, apoptosis was first induced by exposure to a synthetic peptide homologous to residues 106–126 of the human prion protein (PrP), PrP106–126. Exposure to its aggregated form induced a massive neuronal death within 24 h. Apoptosis was characterized by nuclear fragmentation, neuritic retraction and fragmentation and activation of caspase‐3. During the early decision phase, reactive oxygen species were detected after 3 h. Using immunocytochemistry, we showed a peak of phosphorylated c‐Jun–N‐terminal kinase (JNK) translocation into the nucleus after 8 h, along with the activation of the nuclear c‐Jun transcription factor. Both pharmacological inhibition of JNK by SP600125 and overexpression of a dominant negative form of c‐Jun significantly reduced neuronal death, while the MAPK p38 inhibitor SB203580 had no effect. Apoptosis was also studied after exposure of tg338 cortical neurons in primary culture to sheep scrapie agent. In this model, prion‐induced neuronal apoptosis gradually increased with time and induced a 40% cell death after 2 weeks exposure. Immunocytochemical analysis showed early c‐Jun activation after 7 days. In summary, the JNK–c‐Jun pathway plays an important role in neuronal apoptosis induced by PrP106–126. This pathway is also activated during scrapie infection and may be involved in prion‐induced neuronal death. Pharmacological blockade of early pathways opens new therapeutic prospects for scrapie PrP‐based pathologies.
Recognition memory impairment and brain oxidative stress induced by postnatal iron administration
Authors: De Lima Maria Noemia M. , Polydoro Manuela , Laranja Daniela C. , Bonatto Fernanda , Bromberg Elke , Moreira José Cláudio F. , Dal‐Pizzol Felipe , Schröder Nadja 
Published: May 2005

AbstractIron accumulation in the brain has been implicated in the pathogenesis of neurodegenerative disorders. It is known that iron catalyses the formation of highly reactive hydroxyl radicals. Recent studies have implicated oxidative damage in memory deficits in rats and humans. The purpose of the present study was to investigate the long‐term effects of iron treatment in four different phases of the neonatal period on recognition memory in rats. Additionally, parameters of oxidative stress in cerebral regions related to memory formation were evaluated. Male Wistar rats received vehicle or 10.0 mg/kg of Fe2+ orally at postnatal days 5–7, 12–14, 19–21 or 30–32. Animals given iron at any phase of the neonatal period showed impairments in long‐term retention of object recognition memory, although only the group given iron from postnatal days 12–14 showed a complete memory blockade. Iron treatment induced oxidative damage in the brain as assessed by the thiobarbituric acid reactive species assay. Moreover, iron administration increased superoxide production in submitochondrial particles, suggesting impaired mitochondrial function; and there was an increase in superoxide dismutase activity in brain regions susceptible to iron administration. The results show that iron load in the early stages of life induces cognitive impairment possibly by inducing oxidative damage in the brain. These findings are consistent with the view that oxidative stress may be related to the cognitive decline observed in normal ageing.
KCC2 expression in immature rat cortical neurons is sufficient to switch the polarity of GABA responses
Authors: Lee Hanmi , Chen Carol Xiu‐Qing , Liu Yong‐Jian , Aizenman Elias , Kandler Karl 
Published: May 2005

AbstractDuring brain development, GABA and glycine switch from being depolarizing to being hyperpolarizing neurotransmitters. This conversion results from a gradual decrease in the chloride electrochemical equilibrium potential (ECl) of developing neurons, which correlates to an increase in the expression or activity of the potassium chloride cotransporter, KCC2. However, evidence as to whether KCC2 expression is sufficient, in and of itself, to induce this switch is lacking. In order to address this question, we used a gain‐of‐function approach by over‐expressing human KCC2 (hKCC2) in immature cortical neurons, before endogenous up‐regulation of KCC2. We found that premature expression of hKCC2 produced a substantial negative shift in the GABA reversal potential and decreased or abolished GABA‐elicited calcium responses in cultured neurons. We conclude that KCC2 expression is not only necessary but is also sufficient for ending the depolarizing period of GABA in developing cortical neurons.
Patterned firing of parietal cells in a haptic working memory task
Authors: Bodner M. , Shafi M. , Zhou Y.‐D. , Fuster J. M. 
Published: May 2005

AbstractCells in the somatosensory cortex of the monkey are known to exhibit sustained elevations of firing frequency during the short‐term mnemonic retention of tactile information in a haptic delay task. In this study, we examine the possibility that those firing elevations are accompanied by changes in firing pattern. Patterns are identified by the application of a pattern‐searching algorithm to the interspike intervals of spike trains. By sequential use of sets of pattern templates with a range of temporal resolutions, we find patterned activity in the majority of the cells investigated. In general, the degree of patterning significantly increases during active memory. Surrogate analysis suggests that the observed patterns may not be simple linear stochastic functions of instantaneous or average firing frequency. Therefore, during the active retention of a memorandum, the activity of a ‘memory cell’ may be characterized not only by changes in frequency but also by changes in pattern.
Autonomic fibre sprouting and changes in nociceptive sensory innervation in the rat lower lip skin following chronic constriction injury
Authors: Grelik C. , Bennett G. J. , Ribeiro‐da‐Silva A. 
Published: May 2005

AbstractIn this study we used immunocytochemistry to investigate whether autonomic fibres sprouted in the skin of the lower lip in a rat model of neuropathic pain. We used a bilateral chronic constriction injury (CCI) of the mental nerve (MN), a branch of the trigeminal nerve. In this model, we also studied the accompanying changes in peptidergic [calcitonin gene‐related peptide (CGRP)‐immunoreactive] sensory fibres, as well as in trkA receptor immunoreactivity in the sensory nerves. Autonomic (sympathetic and parasympathetic) fibre sprouting was first observed 1 week post‐injury with a peak in the number of sprouted fibres occurring at 4 and 6 weeks post‐CCI. CGRP‐IR fibres almost disappeared at 2 weeks post‐CCI, but quickly sprouted, leading to a significant peak above sham levels 4 weeks post‐injury. trkA receptor expression was found to be up‐regulated in small cutaneous nerves 4 weeks post‐CCI, returning to sham levels by 8 weeks post‐CCI. There was no sympathetic fibre sprouting in the trigeminal ganglion following CCI. At 4 weeks post‐CCI, rats displayed spontaneous, directed grooming to the area innervated by the MN that was not seen in sham animals, which we interpreted as a sign of spontaneous pain or dysesthesiae. Collectively, our findings indicate that as a result of autonomic sprouting due to CCI of the MN, remaining intact nociceptive fibres may potentially develop sensitivity to sympathetic and parasympathetic stimulation, which may have a role in the generation of abnormal pain following nerve injury.
Changes in electrophysiological activity in the accessory olfactory bulb and medial amygdala associated with mate recognition in mice
Authors: Binns K. E. , Brennan P. A. 
Published: May 2005

AbstractThe ability of female mice to recognize their mate's pheromonal identity is critical for the maintenance of their pregnancy and is hypothesized to involve increases in the inhibitory control of mitral/tufted projection neurons in the accessory olfactory bulb. Local field potential recordings from this region of freely behaving female mice showed oscillating neural activity over a wide range of frequencies, which was affected by chemosensory input and prior experience. Mating caused lasting increases in the baseline neural activity in the accessory olfactory bulb, with large increases in the amplitude of local field potential oscillations across a range of frequencies. Exposure to the mate's urinary cues remained effective in increasing the power of these oscillations following mating, but urinary cues from an unfamiliar male were ineffective. A differential response to the familiar and unfamiliar chemosignals was also observed at the level of the amygdala following mating. Individual neurons in the medial amygdala responded more strongly to urine from an unfamiliar male than from the mating male. These findings are consistent with the selective enhancement of inhibition of the familiar pheromonal signal at the level of the accessory olfactory bulb, which is proposed to underlie recognition of the mating male.
Ca2+/calmodulin‐dependent protein kinase II in the spinal cord contributes to neuropathic pain in a rat model of mononeuropathy
Authors: Dai Yi , Wang Hu , Ogawa Akiko , Yamanaka Hiroki , Obata Koichi , Tokunaga Atsushi , Noguchi Koichi 
Published: May 2005

AbstractCa2+/calmodulin‐dependent protein kinase II (CaMKII) is known to subserve activity‐dependent neuronal plasticity in the central nervous system. To examine in vivo the implication of spinal CaMKII activity in the generation and development of neuropathic pain after peripheral nerve injury, we used an animal model of mononeuropathy, the chronic constriction injury (CCI) model, in the rat. We found that, 3 days after CCI, the total CaMKII (tCaMKII) immunoreactivity increased in the superficial laminae of the spinal cord and this increase continued for up to 14 days. The immunoreactivity of phosphorylated CaMKII showed an increase from 1 day after CCI, which preceded the up‐regulation of tCaMKII. A non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK801, significantly attenuated the increase of tCaMKII and phosphorylated CaMKII. Moreover, intrathecal administration of an inhibitor of CaMKII, KN93, before the CCI surgery attenuated the development of thermal hyperalgesia and mechanical allodynia. In addition, KN93 significantly reduced the nociceptive behavior in phase II of the formalin test. These findings demonstrate that the activity of CaMKII in spinal neurons is elevated after peripheral nerve injury and may be involved in central sensitization. The alteration of CaMKII is considered to be a neuroplastic change that occurs in spinal neurons that contributes to neuropathic pain, suggesting the potential for the development of novel therapeutics for neuropathic pain that target CaMKII.
Induction of ephrin‐B1 and EphB receptors during denervation‐induced plasticity in the adult mouse hippocampus
Authors: Wang Yan , Ying Guo‐Xin , Liu Xin , Wang Wen‐Yuan , Dong Jing‐Hui , Ni Zi‐Mei , Zhou Chang‐Fu 
Published: May 2005

AbstractIt has been widely demonstrated that Eph receptors and their ephrin ligands play multiple pivotal roles in the development of the nervous system. However, less is known about their roles in the adult brain. Here we reported the expression of ephrin‐B1 and its cognate EphB receptors in the adult mouse hippocampus at 3, 7, 15, 30 and 60 days after transections of the entorhinal afferents. In situ hybridization and immunohistochemistry showed the time‐dependent up‐regulation of ephrin‐B1 in the denervated areas of the hippocampus, which initiated at 3 days postlesion (dpl), reached maximal levels at 7–15 dpl, remained slightly elevated at 30 dpl and recovered to normal levels by 60 dpl. Double labeling of ephrin‐B1 and glial fibrillary acidic protein revealed that ephrin‐B1‐expressing cells in the denervated areas were reactive astrocytes. Furthermore, a ligand‐binding assay using ephrin‐B1/Fc chimera protein also displayed the up‐regulation of EphB receptors in the denervated areas of the hippocampus in a similar manner to that of ephrin‐B1. Within the first week postlesion, the EphB receptors were expressed by reactive astrocytes. After 7 dpl, however, EphB receptors were expressed not only by reactive astrocytes but also first by sprouting axons and later by regrowing dendrites. These results suggest that the ephrin‐B1/EphB system may participate in the lesion‐induced plasticity processes in the adult mouse hippocampus.
Synaptic plasticity in the absence of backpropagating spikes of layer II inputs to layer V pyramidal cells in rat visual cortex
Authors: Stiefel Klaus M. , Tennigkeit Frank , Singer Wolf 
Published: May 2005

AbstractUse‐dependent changes of synaptic transmission are thought to depend on the evaluation of temporal correlations between pre‐ and postsynaptic excitatory activity. Previous studies have demonstrated long‐term potentiation (LTP) in layer V pyramidal cells after coincident pairing of presynaptic excitatory input with postsynaptic depolarizations, evoking backpropagating action potentials (BAPs). Here we paired excitatory layer II input with somatic hyperpolarization, which blocked BAPs in layer V pyramidal cells of rat visual cortex and induced reliable long‐term depression (LTD). Upon cholinergic receptor activation, this BAP‐independent protocol also induced LTP, which was not dependent on N‐methyl‐d‐aspartate receptor activation, but blocked by metabotropic glutamate receptor (mGluR) antagonists.
A dual function for Munc‐18 in exocytosis of PC12 cells
Authors: Schütz Dagmar , Zilly Felipe , Lang Thorsten , Jahn Reinhard , Bruns Dieter 
Published: May 2005

AbstractMunc‐18 interacts with the SNARE protein syntaxin and is supposed to influence transmitter release by controlling the formation of exocytosis‐relevant SNARE complexes. Here, we used combined biochemical and physiological analyses to study the role of the Munc‐18/syntaxin interaction in large dense core vesicle (LDCV) exocytosis of neuroendocrine PC12 cells. We compared two Munc‐18 mutants carrying mutations in the syntaxin‐binding region and show that Munc‐18's membrane association depends on direct binding to syntaxin. The data suggest that perturbation of syntaxin binding inhibits neurotransmitter release upstream of the individual fusion event implying an essential role of the Munc‐18/syntaxin complex leading to exocytosis. Furthermore, we show that a Munc‐18 mutant lacking any syntaxin binding has a stimulatory effect on secretion, and provide evidence that the Munc‐18/Mint1 interaction may constitute a second pathway for Munc‐18 to regulate exocytosis. We propose that Munc‐18 represents a dynamic link between syntaxin‐related and Mint1‐related mechanisms, both involved in the control of LDCV exocytosis in neuroendocrine cells.