bluuebunny/crossref_metadata_2025 huggingface dataset:
Geochemistry of adakitic quartz diorite in the Yamizo Mountains, central Japan: Implications for Early Cretaceous adakitic magmatism in the inner zone of southwest Japan
Authors: Takahashi Yutaka , Kagashima Shin‐Ichi , Mikoshiba Masumi U.
Published: May 2005

Abstract  Small‐volume plutons of Early to Late Cretaceous ages are widely distributed in the Yamizo Mountains, central Japan. These plutons consist predominantly of granitoids, classified into hornblende gabbro, quartz diorite, hornblende–biotite granodiorite and coarse‐grained biotite granite. The quartz diorite (52–64 wt% of SiO2) is characterized by a high Sr content (606–769 p.p.m.) associated with a low Y (13–27 p.p.m.) and heavy rare earth element content (Yb content of 1.19–2.13 p.p.m.). On the Sr/Y versus Y diagram, this rock type mainly plots in the adakite and Archean high‐Al tonalite, trondhjemite and granodiorite (TTG) field. Together with its initial Sr isotopic ratios, which range from 0.7038 to 0.7046, these data suggest that quartz diorite originated as slab melts. However, geochemical calculations assuming either eclogite or garnet amphibolite as the source material do not support this suggestion. Instead, the chemical compositions of quartz diorite are better explained by the fractional crystallization of hornblende, plagioclase and biotite from a primitive, basaltic melt in a magma chamber. In this case, the formation of the associated hornblende gabbro can also be explained by the accumulation of hornblende and plagioclase. Adakitic rocks of Early Cretaceous ages have also been reported in the Tamba Belt of the inner zone of southwest Japan, located ca 500 km west of the Yamizo Mountains. These rocks can be correlated to the adakitic rocks in the Yamizo Mountains based on the geology, petrography, geochemistry and radiometric ages. Therefore, we propose the possibility that the Early Cretaceous adakitic rocks in the inner zone of southwest Japan were produced by fractional crystallization from basaltic arc magmas generated by a partial melting of metasomatized wedge mantle peridotite.
Partial melting controls on the northwest Kyushu basalts from Saga‐Futagoyama
Authors: Mashima Hidehisa
Published: May 2005

Abstract  The major element and compatible trace element compositions of the northwest Kyushu basalts (NWKBs) collected from Saga‐Futagoyama were analyzed to examine the petrogenesis of these basalts. Although nepheline‐normative alkaline basalts are not found in the basalts from Saga‐Futagoyama, the Saga‐Futagoyama basalts almost cover the major element variations of NWKBs. The basalts can be chemically divided into two groups: an Fe‐poor group (IPG) and an Fe‐rich group (IRG). The compositional variation of IPG basalts is essentially controlled by the partial melting of the source as suggested by the following: (i) bulk rock MgO, FeO and NiO compositions indicate that some IPG samples were equilibrated with mantle olivine; and (ii) correlations between Al2O3, CaO and MgO are consistent with those of experimental partial melts of peridotites. The inconsistent behaviors of the elements compatible with clinopyroxene (Cpx), such as V (Sc and Cu), preclude the significant role of the fractional crystallization of Cpx and spinel in IPG variation. IPG basalts have low Al and high Fe concentrations compared to the products of melting experiments involving peridotites and pyroxenites, suggesting that the IPG source would have a lithology and bulk rock composition different from those of typical peridotites and pyroxenites. IRG basalts have negative correlations between Fe2O3* and MgO, and between V and Fe2O3*/MgO, indicating that IRG basalts would have fractionated Cpx. However, the anomalously Fe‐rich feature of IRG basalts compared with NWKBs collected from other areas suggests that the role of Cpx fractionation in NWKBs is minor. Relatively low melting temperatures would have principally caused the large chemical variation of NWKBs.
Cholinergic and noncholinergic brainstem neurons expressing Fos after paradoxical (REM) sleep deprivation and recovery
Authors: Verret Laure , Léger Lucienne , Fort Patrice , Luppi Pierre‐Hervé
Published: May 2005

It is well accepted that populations of neurons responsible for the onset and maintenance of paradoxical sleep (PS) are restricted to the brainstem. To localize the structures involved and to reexamine the role of mesopontine cholinergic neurons, we compared the distribution of Fos‐ and choline acetyltransferase‐labelled neurons in the brainstem of control rats, rats selectively deprived of PS for ≈ 72 h and rats allowed to recover from such deprivation. Only a few cholinergic neurons from the laterodorsal (LDTg) and pedunculopontine tegmental nuclei were Fos‐labelled after PS recovery. In contrast, a large number of noncholinergic Fos‐labelled cells positively correlated with the percentage of time spent in PS was observed in the LDTg, sublaterodorsal, alpha and ventral gigantocellular reticular nuclei, structures known to contain neurons specifically active during PS. In addition, a large number of Fos‐labelled cells were seen after PS rebound in the lateral, ventrolateral and dorsal periaqueductal grey, dorsal and lateral paragigantocellular reticular nuclei and the nucleus raphe obscurus. Interestingly, half of the cells in the latter nucleus were immunoreactive to choline acetyltransferase. In contrast to the well‐accepted hypothesis, our results strongly suggest that neurons active during PS, recorded in the mesopontine cholinergic nuclei, are in the great majority noncholinergic. Our findings further demonstrate that many brainstem structures not previously identified as containing neurons active during PS contain cholinergic or noncholinergic neurons active during PS, and these structures may therefore play a key role during this state. Altogether, our results open a new avenue of research to identify the specific role of the populations of neurons revealed, their interrelations and their neurochemical identity.
Abnormal activation of face processing systems at early and intermediate latency in individuals with autism spectrum disorder: a magnetoencephalographic study
Authors: Bailey Anthony J. , Braeutigam Sven , Jousmäki Veikko , Swithenby Stephen J.
Published: May 2005

The neurological basis of developmental psychopathology in autism is a matter of intense debate. Magnetoencephalography (MEG) was used to study the neuronal responses associated with the processing of faces in 12 able adults with autism spectrum disorders (ASD), performing image categorization and image identification tasks. The neuromagnetic data were analysed using nonparametric time‐series analysis and equivalent current dipole estimation. Comparison data were obtained from 22 normally developing adults. In individuals with ASD, the neural responses to images of faces, observed in right extrastriate cortices at ≈ 145 ms after stimulus onset, were significantly weaker, less lateralized and less affected by stimulus repetition than in control subjects. Early latency (30–60 ms) responses to face images, over right anterior temporal regions, differed significantly between the two subject groups in the image identification task. No such difference was observed for images of mugs or meaningless geometrical patterns. These findings suggest that, during the course of development in individuals with ASD, the cortical activity associated with the processing of human faces assumes a different‐from‐normal localization in extrastriate brain regions. This abnormal localization may be associated with unusual, but nevertheless face‐specific, fast processing pathways.
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

If 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

Using 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

This 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

Neuroactive 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

Prion 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

Iron 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

During 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

Cells 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

In 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

The 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

Ca2+/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

It 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

Use‐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

Munc‐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.
Voltage‐gated Ca2+ channel subtypes mediating GABAergic transmission in the rat supraoptic nucleus
Authors: Bhaukaurally Khaleel , Panatier Aude , Poulain Dominique A. , Oliet Stéphane H. R.
Published: May 2005

The supraoptic nucleus receives an abundant γ‐aminobutyric acid (GABA)ergic input which is inhibited by activation of various presynaptic metabotropic receptors. We here analysed the subtypes of voltage‐gated Ca2+ channels intervening in the control of transmitter release at these synapses. To address this issue, we tested various specific inhibitors of Ca2+ channels on evoked inhibitory postsynaptic currents (IPSCs). Blocking N‐ and P‐type voltage‐gated Ca2+ channels with 1 µmω‐conotoxin‐GVIA and 20 nmω‐agatoxin‐IVA, respectively, dramatically reduced IPSC amplitude. Q‐ and l‐type Ca2+ channels also contributed to GABAergic transmission, although to a lesser extent, as revealed by applications of 200 nmω‐agatoxin‐IVA and of the dihydropyridines nifedipine (10 µm) and nimodipine (10 µm). Evoked IPSCs were insensitive to SNX‐482 (300 nm), a blocker of some R‐type Ca2+ channels. Analysis of selective blockade by the various antagonists suggested that multiple types of Ca2+ channels synergistically interact to trigger exocytosis at some individual GABA release sites. We next investigated whether inhibition of GABA release in response to the activation of metabotropic glutamate, GABA and adenosine receptors involved the modulation of these presynaptic Ca2+ channels. This was not the case, as the inhibitory actions of selective agonists of these receptors were unaffected by the presence of the different Ca2+ channel antagonists. This finding suggests that these metabotropic receptors modulate GABAergic transmission through a different mechanism, downstream of Ca2+ entry in the terminals, or upstream through the activation of K+ channels.
Perioperative management of face‐to‐face craniopagus twins separation
Authors: PIETRINI D. , VALENTI M. , PUSATERI A. , SCORZONI M. , TOSI F. , FORTE E. , BARBI S. , CARESTA E. , CALDARELLI M. , DI ROCCO C. , PIASTRA M.
Published: May 2005

Craniopagus conjoining represents a complex and challenging issue for neurosurgeons as well as for anesthesiologists. A rare face‐to‐face case of conjoined twins underwent surgical separation and presented peculiar differences compared with those already reported in the literature. Even in cases lacking large cerebrovascular sinus connections, the impending risk of large blood loss and hemorrhagic shock in the infant requires a high level of surveillance and the institution of invasive monitoring.
Caudal anesthesia for minor pediatric surgery: a prospective randomized comparison of ropivacaine 0.2% vs levobupivacaine 0.2%
Authors: IVANI G. , DE NEGRI P. , LONNQVIST P.A. , L'ERARIO M. , MOSSETTI V. , DIFILIPPO A. , ROSSO F.
Published: May 2005

Background : Previous published data comparing ropivacaine 0.2% with levobupivacaine 0.25% have suggested that ropivacaine might be associated with less early postoperative motor blockade compared with levobupivacaine. The aim of the present study was to further investigate this issue comparing equal concentrations (0.2%) of ropivacaine and levobupivacaine in children undergoing minor subumbilical surgery.

Methods : Following induction of a standardized anesthetic, patients (1–7 years) were randomized in a double‐blind manner to receive a caudal block with either ropivacaine 0.2% (group R, n = 30) or levobupivacaine 0.2% (group L, n = 30), total volume 1 ml·kg−1. Motor blockade (modified Bromage scale; primary end‐point) and analgesia [Children and Infants Postoperative Pain Scale (CHIPPS) score] were assessed at predetermined time points during the first 24‐postoperative hours.

Results : Motor blockade was only registered during the first postoperative hour with no significant differences between the groups (group R n = 5, group L n = 8). Postoperative CHIPPS scores were almost identical in both groups with only seven and six patients requiring supplemental analgesia (CHIPPS score ≥4) in the R and L groups, respectively.

Conclusions : A 0.2% concentrations of ropivacaine or levobupivacaine are clinically very similar with regard to postoperative analgesia and unwanted postoperative motor blockade in children undergoing minor subumbilical surgery.
Anesthetic management of a neonate with vein of Galen aneurysmal malformations and severe pulmonary hypertension
Authors: ASHIDA YUKI , MIYAHARA HIROMI , SAWADA HIROHUMI , MITANI YOSHIHIDE , MARUYAMA KAZUO
Published: May 2005

Vein of Galen aneurysmal malformations (VGAMs) are rare congenital vascular malformations and excessive arteriovenous shunt causes intractable congestive high‐output heart failure in the neonate. We report a case of successful staged transcatheter embolizations for a neonate with congestive heart failure and pulmonary hypertension (PH). Heart failure was dramatically relieved as the staged procedure progressed. Although transcatheter embolizations is essential for the treatment, inhaled nitric oxide (iNO) was helpful as a bridge treatment to reduce right‐to‐left shunt before the initial emergency embolization. Endovascular embolization is a less invasive therapy than open cranial surgery and allows hemodynamic stability. Perioperative iNO can be used to manage PH in VGAMs.
Anesthesia for a neonate with persistent buccopharyngeal membrane and unilateral choanal atresia
Authors: LIM EVANGELINE H. , TAN SHANI , LIM SUAN‐LING
Published: May 2005

We report our anesthetic management of a neonate who presented with complete persistent buccopharyngeal membrane and unilateral choanal atresia, and underwent examination under anesthesia. Maintaining airway patency and spontaneous respiration were our priority. Intravenous propofol was used to maintain adequate anesthetic depth for flexible laryngotracheoscopy and nasotracheal intubation through the only patent passage. We encountered problems of bradycardia and hypotension. Tracheostomy was performed. Definitive management of the persistent buccopharyngeal membrane was carried out on day 14.
Intraoperative low‐dose S‐ketamine has no preventive effects on postoperative pain and morphine consumption after major urological surgery in children
Authors: BECKE KARIN , ALBRECHT SVEN , SCHMITZ BERND , RECH DORIT , KOPPERT WOLFGANG , SCHÜTTLER JÜRGEN , HERING WERNER
Published: May 2005

Background : Clinical studies suggest low‐dose ketamine may have preemptive effects on postoperative pain in adults. The objective of this study was to determine whether intraoperative low‐dose S‐ketamine reduces postoperative pain and morphine consumption in children undergoing major urological surgery.

Materials : Thirty children scheduled for major urological surgery were included in this prospective study. Anesthesia was performed as total intravenous anesthesia (TIVA) with alfentanil and propofol. Fifteen patients additionally received an intravenous bolus of S‐ketamine (0.2 mg·kg−1) followed by a continuous infusion of 5 μg·kg−1·min−1, which was stopped immediately after skin closure (Ketamine Group). Another 15 patients received an infusion of saline (Control group). After transfer to the PACU, pain intensity was evaluated using a numeric rating scale (NRS). First patient controlled analgesia (PCA) request, cumulative morphine consumption and pain intensities within the first 72 h were compared.

Results : Morphine consumption was not significantly different during the first 72 h (Control: 0.4 mg·kg−1, 0.24–0.51 mg·kg−1, Ketamine: 0.32 mg·kg−1, 0.19–0.61 mg·kg−1; median, 25–75% percentile; n.s.). However, differences were found in pain intensity during the first postoperative hour (Control: 4.0, 3.2–4.6, Ketamine: 2.5, 1.3–3.5; median, 25–75% percentile; P < 0.05) and in the time to first PCA use (Control: 37, 28–46 min, Ketamine: 62, 38–68 min; median, 25–75% percentile; P < 0.05).

Conclusions : Intraoperative low‐dose S‐ketamine had no effect on morphine consumption during the first 72 h after surgery. The differences in pain intensity and time to first PCA use probably reflect additional sedation and antinociceptive effects of S‐ketamine rather than a true ‘prevention’ of pain.
The addition of clonidine 2 μg·kg−1 does not enhance the postoperative analgesia of a caudal block using 0.125% bupivacaine and epinephrine 1 : 200 000 in children: a prospective, double‐blind, randomized study1
Authors: WHEELER MELISSA , PATEL ARTI , SURESH SANTHANAM , ROTH ANDREW G. , BIRMINGHAM PATRICK K. , HEFFNER CORRI L. , COTÉ CHARLES J.
Published: May 2005

Background : In this prospective, randomized, double‐blind study, we compared the efficacy of 0.125% bupivacaine and epinephrine 1 : 200 000 with and without clonidine 2 μg·kg−1 for ‘single shot’ pediatric caudal analgesia.

Methods : Thirty ASA I and II children, ages 2–8 years, undergoing outpatient surgical procedures below the umbilicus received 1 ml·kg−1 0.125% bupivacaine with fresh epinephrine 1 : 200 000 and clonidine 2 μg·kg−1 (group‐C) or 1 ml·kg−1 0.125 % bupivacaine with epinephrine 1 : 200 000 (group‐NC). All patients received a standardized general anesthetic (induction with 67% N2O in O2 and sevoflurane followed by isoflurane maintenance). Primary outcome measures were time to first rescue analgesic and number of patients requiring rescue analgesic at 4, 6, 8, 12, and 24 h after caudal placement. Secondary outcome measures included: extubation times, Objective Pain Scale (OPS) scores, sedation scores, time in postanesthesia care unit (PACU), discharge time, number of analgesic doses given in 24 h following caudal blockade, and adverse effects (vomiting, hypotension, and bradycardia).

Results : There were no differences in demographics, investigated parameters, or adverse effects between groups.

Conclusions : We found that the addition of clonidine 2 μg·kg−1 to 0.125% bupivacaine with fresh epinephrine 1 : 200 000 for caudal analgesia did not significantly delay the time to first rescue analgesic or decrease the overall need for rescue analgesics in children 2–8 years undergoing surgical procedures below the umbilicus.
Severe hemoptysis in a child after the Fontan procedure
Authors: DEISENBERG MARKUS , STAYER STEPHEN A.
Published: May 2005

There is an increased incidence of pulmonary hemorrhage and hemoptysis among patients with congenital heart disease (CHD). The pathophysiology of pulmonary hemorrhage in CHD includes pulmonary hypertension, pulmonary venous congestion, aorto‐pulmonary collaterals, pulmonary arteriovenous malformations, and dilated bronchial arteries. We present the case of a 6‐year old boy who required treatment for massive hemoptysis after staged palliation for hypoplastic left heart syndrome (HLHS). Effective management of this life threatening entity is described as well as the anesthetic implications of performing rigid bronchoscopy in a patient with the Fontan circulation and massive hemoptysis.
Herbal and homeopathic medication use in pediatric surgical patients
Authors: EVERETT LUCINDA L. , BIRMINGHAM PATRICK K. , WILLIAMS GLYN D. , RANDALL BRENN B. , SHAPIRO JAY H.
Published: May 2005

Background : Patients who present for surgery may be using herbal or homeopathic preparations; adverse effects of some of these substances include bleeding, cardiovascular changes, and liver dysfunction. Little information is available on the frequency of use in the pediatric surgical population.

Methods : With institutional approval, a survey was conducted to assess the use of vitamins, nutritional supplements, or herbal or homeopathic preparations in children presenting for surgery in five geographically diverse centers in the USA.

Results : A total of 894 completed surveys showed that overall, 3.5% of pediatric surgical patients had been given herbal or homeopathic medications in the 2 weeks prior to surgery. Most substances were prescribed by parents. The use of these medications did not differ between children with coexisting diseases and those without; use was also not different among ethnic groups or by residence setting (city, suburban, rural). There was a significant difference between the west coast centers in the study compared with the rest of the country (7.5% of patients in Palo Alto, CA; 5.5% of patients in Seattle, WA; 1.5% of patients in Chicago, IL; and 1.9% in Virginia and Delaware used herbal or homeopathic remedies). The most prevalent substance given to children presenting for elective surgery was Echinacea.

Conclusions : Herbal and homeopathic medications are used by a small percentage of pediatric patients presenting for elective pediatric surgery patients. Use of these substances should be addressed in the preoperative history.
A noninvasive estimation of mixed venous oxygen saturation using near‐infrared spectroscopy by cerebral oximetry in pediatric cardiac surgery patients
Authors: TORTORIELLO TIA A. , STAYER STEPHEN A. , MOTT ANTONIO R. , DEAN McKENZIE E. , FRASER CHARLES D. , ANDROPOULOS DEAN B. , CHANG ANTHONY C.
Published: May 2005

Background : Near‐infrared spectroscopy (NIRS) is a noninvasive optical monitor of regional cerebral oxygen saturation (rSO2). The aim of this study was to validate the use of NIRS by cerebral oximetry in estimating invasively measured mixed venous oxygen saturation (SvO2) in pediatric postoperative cardiac surgery patients.

Methods : Twenty patients were enrolled following cardiac surgery with intraoperative placement of a pulmonary artery (PA) or superior vena cava (SVC) catheter. Five patients underwent complete biventricular repair – complete atrioventricular canal (n = 3) and other (n = 2). Fifteen patients with functional single ventricle underwent palliative procedures – bidirectional Glenn (n = 11) and Fontan (n = 4). Cerebral rSO2 was monitored via NIRS (INVOS 5100) during cardiac surgery and 6 h postoperatively. SvO2 was measured from blood samples obtained via an indwelling PA or SVC catheter and simultaneously correlated with rSO2 by NIRS at five time periods: in the operating room after weaning from cardiopulmonary bypass, after sternal closure, and in the CICU at 2, 4, and 6 h after admission.

Results : Each patient had five measurements (total = 100 comparisons). SvO2 obtained via an indwelling PA or SVC catheter for all patients correlated with rSO2 obtained via NIRS: Pearson's correlation coefficient of 0.67 (P < 0.0001) and linear regression of r2 = 0.45 (P < 0.0001). Separate linear regression of the complete biventricular repairs demonstrated an r = 0.71, r2 = 0.50 (P < 0.0001). Bland–Altman analysis showed a bias of +3.3% with a precision of 16.6% for rSO2 as a predictor of SvO2 for all patients. Cerebral rSO2 was a more accurate predictor of SvO2 in the biventricular repair patients (bias −0.3, precision 11.8%), compared with the bidirectional Glenn and Fontan patients.

Conclusions : Regional cerebral oximetry via NIRS correlates with SvO2 obtained via invasive monitoring. However, the wide limits of agreement suggest that it may not be possible to predict absolute values of SvO2 for any given patient based solely on the noninvasive measurement of rSO2. Near‐infrared spectroscopy, using the INVOS 5100 cerebral oximeter, could potentially be used to indicate trends in SVO2, but more studies needs to be performed under varying clinical conditions.
Psoas compartment block (PCB) in children: Part II – generation of an institutional learning curve with a new technique1
Authors: SCHUEPFER GUIDO , JÖHR MARTIN
Published: May 2005

Background : Literature concerning institutional learning processes for anesthesia procedures in pediatric anesthesia is rare. Until recently only small series of psoas compartment blocks (PCB) in children have been reported. We report on a series of 100 consecutive blocks using new landmarks and the institutional learning process.

Methods : In 100 consecutive children (5.9–106 kg) PCB was performed using a nerve stimulator. In the lateral position, the needle was inserted between the medial 2/3 and the lateral 1/3 on a line from the spinous process of L4 to the posterior superior iliac spine. Residents unfamiliar with PCB were instructed by one single staff member without manual intervention. Failure was defined as a bloody tap, more than one skin perforation with the needle or relinquishing the procedure to senior staff. To evaluate the institutional learning process the cumulative sum (CUSUM) statistical technique was used. CUSUM analysis was performed using an acceptable failure rate of 10%. A learning curve using a bootstrap technique and a least square fit model was also used.

Results : Although all blocks were clinically successful, only in 64% was a single attempt sufficient. In 16% vascular puncture occurred. Surprisingly the CUSUM analysis showed a clear institutional learning phenomenon. Applying a strict definition for a successful block, more than 100 PCB in an institution may be necessary. Using the generated learning curve, for a success rate of 70% a case load of at least 55 attempts is required.

Conclusions : Although the described new technique had a very high success rate with a low complication rate, PCB in children is not easily implemented into clinical practice when strict criteria of success were used, despite a well‐controlled environment. Training programs could use CUSUM to track the progress of their institutional learning in order to guarantee adequate experience.