bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fast foods – are they a risk factor for asthma?
Authors: Wickens K. , Barry D. , Friezema A. , Rhodius R. , Bone N. , Purdie G. , Crane J. 
Published: November 2005

Background:  Lifestyle changes over the last 30 years are the most likely explanation for the increase in allergic disease over this period.Aim:  This study tests the hypothesis that the consumption of fast food is related to the prevalence of asthma and allergy.Methods:  As part of the International Study of Asthma and Allergies in Childhood (ISAAC) a cross‐sectional prevalence study of 1321 children (mean age = 11.4 years, range: 10.1–12.5) was conducted in Hastings, New Zealand. Using standard questions we collected data on the prevalence of asthma and asthma symptoms, as well as food frequency data. Skin prick tests were performed to common environmental allergens and exercise‐induced bronchial hyperresponsiveness (BHR) was assessed according to a standard protocol. Body mass index (BMI) was calculated as weight/height2 (kg/m2) and classified into overweight and obese according to a standard international definition.Results:  After adjusting for lifestyle factors, including other diet and BMI variables, compared with children who never ate hamburgers, we found an independent risk of hamburger consumption on having a history of wheeze [consumption less than once a week (OR = 1.44, 95% CI: 1.06–1.96) and 1+ times a week (OR = 1.65, 95% CI: 1.07–2.52)] and on current wheeze [consumption less than once a week (OR = 1.17, 95% CI: 0.80–1.70) and 1+ times a week (OR = 1.81, 95% CI: 1.10–2.98)]. Takeaway consumption 1+ times a week was marginally significantly related to BHR (OR = 2.41, 95% CI: 0.99–5.91). There was no effect on atopy.Conclusions:  Frequent consumption of hamburgers showed a dose‐dependent association with asthma symptoms, and frequent takeaway consumption showed a similar association with BHR.
Tectal neurons signal impending collision of looming objects in the pigeon
Authors: Wu Le‐Qing , Niu Yu‐Qiong , Yang Jin , Wang Shu‐Rong 
Published: November 2005

AbstractAlthough the optic tectum in non‐mammals and its mammalian homolog, the superior colliculus, are involved in avoidance behaviors, whether and how tectal neurons respond to an object approaching on a collision course towards the animal remain unclear. Here we show by single unit recording that there exist three classes of looming‐sensitive neurons in the pigeon tectal layer 13, which sends looming information to the nucleus rotundus or to the tectopontine system. The response onset time of tau cells is approximately constant whereas that for rho and eta cells depends on the square root of the diameter/velocity ratio of objects looming towards the animal, the cardioacceleration of which is also linearly related to the square root of this ratio. The receptive field of tectal cells is composed of an excitatory center and an inhibitory periphery, and this periphery does not inhibit responses to looming stimuli. These results suggest that three classes of tectal neurons are specified for detecting an object approaching on a collision course towards the animal, and that rho and eta cells may signal early warning of impending collision whereas tau cells initiate avoidance responses at a constant time before collision through the tectopontine system.
Oxygen and glucose deprivation induces major dysfunction in the somatosensory cortex of the newborn rat
Authors: Albrecht Juliane , Hanganu Ileana L. , Heck Nicolas , Luhmann Heiko J. 
Published: November 2005

AbstractThe mechanisms and functional consequences of ischemia‐induced injury during perinatal development are poorly understood. Subplate neurons (SPn) play a central role in early cortical development and a pathophysiological impairment of these neurons may have long‐term detrimental effects on cortical function. The acute and long‐term consequences of combined oxygen and glucose deprivation (OGD) were investigated in SPn and compared with OGD‐induced dysfunction of immature layer V pyramidal cortical neurons (PCn) in somatosensory cortical slices from postnatal day (P)0–4 rats. OGD for 50 min followed by a 10–24‐h period of normal oxygenation and glucose supply in vitro or in culture led to pronounced caspase‐3‐dependent apoptotic cell death in all cortical layers. Whole‐cell patch‐clamp recordings revealed that the majority of SPn and PCn responded to OGD with an initial long‐lasting ischemic hyperpolarization accompanied by a decrease in input resistance (Rin), followed by an ischemic depolarization (ID). Upon reoxygenation and glucose supply, the recovery of the membrane potential and Rin was followed by a Na+/K+‐ATPase‐dependent postischemic hyperpolarization, and in almost half of the investigated SPn and PCn by a postischemic depolarization. Whereas neither a moderate (2.5 mm) nor a high (4.8 mm) increase in extracellular magnesium concentration protected the SPn from OGD‐induced dysfunction, blockade of NMDA receptors with MK‐801 led to a significant delay and decrease of the ID. Our data demonstrate that OGD induces apoptosis and a profound dysfunction in SPn and PCn, and underline the critical role of NMDA receptors in early ischemia‐induced neuronal damage.
Short‐term constant light potentiation of large‐magnitude circadian phase shifts induced by 8‐OH‐DPAT: effects on serotonin receptors and gene expression in the hamster suprachiasmatic nucleus
Authors: Duncan Marilyn J. , Franklin Kathleen M. , Davis Verda A. , Grossman Gregory H. , Knoch Megan E. , Glass J. David 
Published: November 2005

AbstractNonphotic phase‐shifting of mammalian circadian rhythms is thought to be mediated in part by serotonin (5‐HT) acting in the suprachiasmatic nucleus (SCN) circadian clock. Previously we showed that brief (1–3 days) exposure to constant light (LL) greatly potentiates nonphotic phase‐shifting induced by the 5‐HT agonist, (±)2‐dipropyl‐amino‐8‐hydroxyl‐1,2,3,4‐tetrahydronapthalene (8‐OH‐DPAT). Here we investigated potential mechanisms for this action of LL, including 5‐HT receptor upregulation and SCN clock gene and neuropeptide gene expression. Autoradiographic analysis of ritanserin inhibition of [3H]8‐OH‐DPAT binding indicated that LL (∼2 days) did not affect 5‐HT7 receptor binding in the SCN or dorsal raphe. Measurement of 5‐HT1A autoreceptors in the median raphe and 5‐HT1B receptors in the SCN also showed no effect of LL. In experiment 2, hamsters held under a 14‐h light : 10‐h dark photocycle (LD) or exposed to LL for ∼2 days received an intraperitoneal injection of 8‐OH‐DPAT or vehicle at zeitgeber time (ZT) 6 or 0 and were killed after 2 h of dark exposure. 8‐OH‐DPAT suppressed SCN Per1 and Per2 mRNAs at both ZTs, as assessed by in situ hybridization. Per1 mRNA was also suppressed by LL alone. In addition, in situ hybridization of arginine vasopressin (AVP) mRNA and vasoactive intestinal polypeptide mRNA showed that LL significantly suppressed the former but not the latter. The LL‐induced suppression of SCN Per1 mRNA and AVP mRNA may be involved in LL‐induced potentiation of pacemaker resetting, especially as these data provide additional evidence that LL suppresses circadian pacemaker amplitude, thus rendering the clock more susceptible to phase‐shifting stimuli.
Species and strain differences in the expression of a novel glutamate‐modulating cannabinoid receptor in the rodent hippocampus
Authors: Hoffman Alexander F. , Macgill Alice M. , Smith Dennison , Oz Murat , Lupica Carl R. 
Published: November 2005

AbstractA novel, non‐CB1 cannabinoid receptor has been defined by the persistence of inhibition of glutamatergic EPSPs by the cannabinoid receptor agonist WIN55,212‐2 in mice lacking the cloned CB1 receptor (CB1–/–) (Hajos et al., 2001). This novel receptor was also distinguished from CB1 by its sensitivity to the antagonist SR141716A and its insensitivity to the antagonist AM251 (Hajos & Freund, 2002). We have chosen to refer to this putative receptor as CBsc due to its identification on Schaffer collateral axon terminals in the hippocampus. We examined properties of CBsc receptors in Sprague Dawley (SD) rats and two strains of wild‐type (WT) mice (C57BL/6J and CD1) used as backgrounds for two independent lines of CB1–/– mice (Ledent et al., 1999; Zimmer et al., 1999). The inhibition of synaptic glutamate release by WIN55,212‐2 was observed in hippocampal slices from WT CD1 mice and SD rats but was absent in WT C57 mice. We also found that AM251 and SR141716A antagonized the effect of WIN55,212‐2 in hippocampal slices from CD1 mice and SD rats demonstrating a lack of selectivity of these ligands for CB1 and CBsc receptors in these animals. The results indicate that the glutamate‐modulating CBsc cannabinoid receptor is present in the hippocampi of CD1 mice and SD rats but not in C57BL/6J mice. Thus, we have identified animal models that may permit the study of cannabinoids independently of the novel CBsc receptor (C57CB1+/+), the CBsc receptor independently of the cloned CB1 receptor (CD1CB1–/–), or in the absence of both receptors (C57CB1–/–).
Unilateral lesion of the pedunculopontine nucleus induces hyperactivity in the subthalamic nucleus and substantia nigra in the rat
Authors: Breit S. , Lessmann L. , Benazzouz A. , Schulz J. B. 
Published: November 2005

AbstractRecent data suggest a role for the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease. Although there is anatomical evidence that the PPN and the basal ganglia are reciprocally connected, the functional importance of these connections is poorly understood. Lesioning of the PPN was shown to induce akinesia in primates, whereas in the 6‐hydroxydopamine rat model the PPN was found to be hyperactive. As both nigrostriatal dopamine depletion and lesioning of the PPN were shown to induce akinesia and parkinsonism, the present study was performed in order to investigate the changes in neuronal activity of the subthalamic nucleus (STN) and the substantia nigra pars reticulata (SNr) after unilateral ibotenic acid lesioning of the PPN and after unilateral 6‐hydroxydopamine lesioning of the substantia nigra pars compacta (SNc). The firing rate of STN neurones significantly increased from 10.2 ± 6.2 (mean ± SD) to 14.6 ± 11.7 spikes/s after lesion of the PPN and to 18.6 ± 14.5 spikes/s after lesion of the SNc. The activity of the SNr significantly increased from 19.6 ± 10.5 to 28.7 ± 13.4 spikes/s after PPN lesioning and to 23.5 ± 10.8 spikes/s after SNc lesioning. Furthermore, PPN lesion decreased the number of spontaneously firing dopaminergic SNc cells, while having no effect on their firing rate. The results of our study show that lesion of the PPN leads to hyperactivity of the STN and SNr, similar to the changes induced by lesion of the SNc. Moreover, the decreased activity of SNc cells observed after PPN lesion might be at the origin of activity changes in the STN and SNr.
Identification of an ectodomain within the LAR protein tyrosine phosphatase receptor that binds homophilically and activates signalling pathways promoting neurite outgrowth
Authors: Yang Tao , Yin Weining , Derevyanny Vicki D. , Moore Laura A. , Longo Frank M. 
Published: November 2005

AbstractElucidation of mechanisms by which receptor protein tyrosine phosphatases (PTPs) regulate neurite outgrowth will require characterization of ligand–receptor interactions and identification of ligand‐induced signalling components mediating neurite outgrowth. The first identified ligand of the leucocyte common antigen‐related (LAR) receptor PTP consists of a 99‐residue ectodomain isoform, termed LARFN5C, which undergoes homophilic binding to LAR and promotes neurite outgrowth. We employed peptide mapping of LARFN5C to identify an active neurite‐promoting domain of LAR. A peptide mimetic consisting of 37 residues (L59) and corresponding to the fifth LAR fibronectin type III (FNIII) domain prevented LARFN5C homophilic binding, demonstrated homophilic binding to itself and promoted neurite outgrowth of mouse E16–17 hippocampal neurons and of dorsal root ganglia explants. Response to L59 was partially lost when using neurons derived from LAR‐deficient (–/–) mice or neurons treated with LAR siRNA, consistent with homophilic interaction of L59 with LAR. L59 neurite‐promoting activity was decreased in the presence of inhibitors of Src, Trk, PLCγ, PKC, PI3K and MAPK. L59 activated Src (a known substrate of LAR), FAK and TrkB and also activated downstream signalling intermediates including PKC, ERK, AKT and CREB. BDNF augmented the maximal neurite‐promoting activity of L59, a finding consistent with the presence of shared and distinct signalling pathways activated by L59 with BDNF and L59 with TrkB. These studies are the first to identify an ectodomain of LAR (located within the fifth FNIII domain) capable of promoting neurite outgrowth and point to novel approaches for promotion of neurite outgrowth.
Cell type‐specific regulation of RE‐1 silencing transcription factor (REST) target genes
Authors: Hohl Mathias , Thiel Gerald 
Published: November 2005

AbstractRE‐1 silencing transcription factor (REST) is a transcriptional repressor that represses neuronal gene transcription in non‐neuronal cells. REST target genes are expressed in neurons and in neuroendocrine cells. Here, we show that treatment with the histone deacetylase inhibitor trichostatin A (TSA) or expression of a mutant of REST (DP‐REST:ER) that contains a transcriptional activation domain enhanced expression of the REST target genes encoding synaptophysin and secretogranin II in neuronal as well as in neuroendocrine cells. These data indicate that the synaptophysin and secretogranin II genes are similarly regulated in neuronal and neuroendocrine cells. In contrast, expression of the connexin36 gene was inducible by TSA or DP‐REST:ER only in pancreatic α and β cells, but not in neuronal and pituitary cells, indicating that transcriptional repression by REST functions in a cell type‐specific manner. Expression of the BDNF and GluR2 genes, both described as targets of REST, was not induced by either TSA or expression of DP‐REST:ER in neuronal or neuroendocrine cells. Chromatin immunoprecipitation experiments using antibodies directed against methylated histone H3Lys4 or H3Lys9 showed a perfect correlation between expression of REST target genes in different cell types and nucleosomal modifications that distinguish active from inactive genes. We conclude that the cell type‐specific microenvironment, in particular the cell type‐specific structure of the chromatin, is crucial for the ability of REST to control gene transcription.
Photic inhibition of TrkB/Ras activity in the pigeon's tectum during development: impact on brain asymmetry formation
Authors: Manns Martina , Güntürkün Onur , Heumann Rolf , Blöchl Andrea 
Published: November 2005

AbstractAsymmetric photic stimulation during embryonic or post‐hatch development induces a functional lateralization of the pigeon's visual system, which is accompanied by left–right differences in tectal cell sizes. The intracellular membrane‐anchored GTPase Ras can be activated by a number of upstream mechanisms including binding of brain‐derived neurotrophic factor to its specific TrkB receptor. Ras activity plays an important morphogenetic role in neurons and therefore might also be involved in the asymmetric differentiation of tectal cells. To investigate the role of Ras, we determined the relative levels of activated Ras and of signalling active phospho‐TrkB in tecta of light‐ and dark‐incubated pigeons and combined this with an immunohistochemical detection of Ras‐GTP and TrkB receptors. While Ras activation levels did not differ between light‐ and dark‐incubated pigeons during embryonic development, directly after hatching Ras activity was significantly decreased in the stronger stimulated left tectum of light‐incubated animals. This was accompanied by lower levels of TrkB phosphorylation. Immunohistochemical staining revealed Ras‐GTP‐positive cell bodies within the efferent cell layer. These cells were TrkB‐positive and developed enlarged soma sizes within the right tectum during the first week after hatching. This association suggests asymmetric Ras activation to be involved in the asymmetric differentiation of the efferent cells as a result of asymmetric TrkB signalling. Because asymmetric light exposure occurs only during embryonic development, the observed transient asymmetric inhibition of TrkB/Ras activity after hatching may reflect differential embryonic maturation of tectal inhibitory circuits leading to a functional superiority of the right eye in the adult organism.
Segregation between acquisition and long‐term memory in sensorimotor learning
Authors: Zach Neta , Kanarek Naama , Inbar Dorrit , Grinvald Yael , Milestein Tomer , Vaadia Eilon 
Published: November 2005

AbstractIt is widely accepted that learning first involves generating new memories and then consolidating them into long‐term memory. Thus learning is generally viewed as a single continuous process with two sequential stages; acquisition and consolidation. Here, we tested an alternative hypothesis proposing that acquisition and consolidation take place, at least partly, in parallel. Human subjects learned two visuomotor tasks. One task required moving a cursor under visuomotor rotation and the other required arbitrary association of colour to direction of movement. Subjects learned the two tasks in sequence, and were tested for acquisition of the second immediately after learning the first, and for retention of the first on the following day. The results show that learning one task led to proactive interference to acquisition of the second. However, this interference was not accompanied by retroactive interference to consolidation of the first task, indicating that acquisition and consolidation can be uncoupled.
Morphine withdrawal‐induced morphological changes in the nucleus accumbens
Authors: Spiga Saturnino , Puddu Maria Cristina , Pisano Milena , Diana Marco 
Published: November 2005

AbstractMorphine withdrawal produces a hypofunction of mesencephalic dopamine neurons that impinge upon medium spiny neurons (MSN) of the forebrain. After chronic treatment (from 20 to 140 mg/kg of morphine twice a day over 14 days at escalating doses) rats were withdrawn from chronic morphine spontaneously and pharmacologically. In these two distinct conditions we studied the effects of withdrawal on the morphology of MSN of the core and shell of the nucleus accumbens (Nacc). MSN were stained with the Golgi–Cox procedure and analysed by a confocal laser‐scanning microscope (CLSM). Our analysis shows that, shell and core MSN differed significantly for perikarya size and spine density, and the various morphine treatments did not affect the perikarya morphometry. Both spontaneous and naloxone‐induced withdrawal produced a similar reduction in spine density in MS shell neurons, as compared with MS core neurons. This effect is selectively localized at the level of second order dendritic trunks where afferents converge. By contrast, spine density counts of accumbens MSN from rats chronically treated with morphine, did not reveal any change. Collectively, the results of the present study are twofold: (i) spontaneous and pharmacologically precipitated withdrawal, but not chronic morphine per se, affects spine density of target structures of a reduced mesolimbic dopamine transmission, and (ii) the reduction of spine density in second order dendritic trunks is selectively segregated in the MSN of the shell of the Nacc. In conclusion, morphine withdrawal dramatically alters spine density, selectively in second order dendritic trunks of Nacc shell MSN, thereby further impoverishing the already abated dopamine (DA) transmission. This is in line with recent views suggesting the hypodopaminergic state as a cardinal feature of opioid dependence.
Vagal pulmonary afferents and central respiratory effects of 5‐HT in newborn rats
Authors: Glérant J.‐Ch. , Khater‐Boidin J. , Salzmann F. , Duron B. 
Published: November 2005

AbstractIn decerebrate newborn rats, serotonin (5‐HT) is a respiratory depressant via activation of 5‐HT2 receptors, whereas it evokes respiratory stimulant effects when applied to the isolated brainstem obtained from the newborn rat. This discrepancy could be due to deafferentation in the in vitro preparation. The aim of our study was to analyse the role of vagal afferents in the modulation of central respiratory effects of 5‐HT. In decerebrate cervically or abdominally bivagotomized newborn rats aged between 0 and 3 days, we recorded electrical activity from the diaphragm and from a hypoglossally innervated tongue muscle, as well as cardiac frequency (Fc), before and after application of 5‐HT to the floor of the IVth ventricle. The effects of related agents (a 5‐HT1A agonist, 8‐OH DPAT, and a 5‐HT2 agonist, DOI) were studied in cervically bivagotomized animals. For comparison, and to assess the spontaneous variability in inspiratory frequency (Fi) and Fc, sham groups were studied. Each group comprised ten newborn rats. In cervically bivagotomized newborn rats, 5‐HT induces a significant increase in Fi, which is the opposite to that observed in decerebrate newborn rats with intact vagi. This respiratory effect is mediated in particular, via activation of 5‐HT1A. By contrast, in abdominally bivagotomized newborn rats, a decrease in Fi was observed in response to 5‐HT (as previously described in decerebrate animals with intact vagi). We conclude that pulmonary vagal afferents modulate the central respiratory action of 5‐HT in decerebrate newborn rats, explaining the conflicting results between in vivo and in vitro experiments.
Expression of netrin‐1, slit‐1 and slit‐3 but not of slit‐2 after cerebellar and spinal cord lesions
Authors: Wehrle Rosine , Camand Emeline , Chedotal Alain , Sotelo Constantino , Dusart Isabelle 
Published: November 2005

AbstractTo determine whether members of the Netrin‐1 and Slit families and their receptors are expressed after central nervous system (CNS) injury, we performed in situ hybridization for netrin‐1, slit‐1, 2 and 3, and their receptors (dcc, unc5h‐1, 2 and 3, robo‐1, 2 and 3) 8 days, 2–3 months and 12–18 months after traumatic lesions of rat cerebellum. The expression pattern of these molecules was unchanged in axotomized Purkinje cells, whereas unc5h3 expression was upregulated in deafferented granule cells. Cells expressing slit‐2 or dcc were never detected at the lesion site. By contrast, cells expressing netrin‐1, slit‐1 and slit‐3, unc5h‐1, 2 and 3, and robo‐1, 2 and 3 (rig‐1) could be detected at the cerebellar lesion site as soon as 8 days after injury. Expression of unc5h‐2, robo‐1, robo‐2, slit‐1 and slit‐3 at the lesion site was maintained until 3 months, and up to 12–18 months for unc5h‐1 and 3 and robo‐3. Likewise, in the mouse spinal cord, netrin‐1, slit‐1 and slit‐3 were also expressed at the lesion site 8 days after injury. Most of the cells expressing these mRNAs were located at the centre of the lesions, suggesting that they are macrophages/activated microglial cells (macrophagic cells) or meningeal fibroblastic cells. The macrophagic nature of most Netrin‐1‐positive cells and the macrophagic or fibroblastic nature of Robo‐1‐positive cells were corroborated by double staining. Thus, Netrin‐1, Slits and their receptors may contribute to the regenerative failure of axons in the adult CNS by inhibiting axon outgrowth or by participating in the formation of the CNS scar.