bluuebunny/crossref_metadata_2025_split huggingface dataset:
“The Island has been Handed over to Me”: Ascension Island as a Company Colony, 1922–42
Authors: Royle Stephen A. 
Published: April 2004

AbstractAscension Island has spent almost all its years of organised human settlement as a military base. The major exception was between 1922 and 1942 when it was ruled by a civilian company, an unusual form of governance in modern colonial history. Though nominally subject to St Helena, and through that British colony to London, outside interference was largely restricted to rulings on colonial etiquette. The manager of the company was also head of both the government and legal systems. This paper considers the operation of this company colony, the tensions between the company and its workforce/subjects, and the contestation from 1942 for political supremacy between the company, the British state and the American forces that arrived when the island became involved in World War II. Ascension's narrative helps to exemplify some themes in postcolonial discourse and, given the unusual and extreme nature of the island's experiences, informatively broadens understanding of colonialism.
Differential targeting of the L‐type Ca2+ channel α1C (CaV1.2) to synaptic and extrasynaptic compartments in hippocampal neurons
Authors: Obermair Gerald J. , Szabo Zsolt , Bourinet Emmanuel , Flucher Bernhard E. 
Published: April 2004

AbstractIn central nervous system neurons L‐type Ca2+ channels are involved in developmental processes, the integration and conduction of postsynaptic electric activity and synaptic plasticity. However, little is known about the channel isoforms underlying each of these functions or about the exact localization and targeting properties of the major L‐type channel isoform α1C (CaV1.2) in neurons. We addressed these questions using high‐resolution immunofluorescence analysis of the endogenous α1C and epitope‐tagged recombinant channel isoforms expressed in mouse hippocampal neurons. Endogenous α1C and surface‐expressed hemagglutinin (HA)‐tagged α1C‐HA were localized in small clusters distributed between the axon initial segment and the apical branches of the dendritic tree. The average cluster size was estimated to be eight channels per α1C‐HA cluster. Analysis of the subcellular localization of α1C‐HA clusters relative to known synaptic markers suggested the existence of two distinct populations of α1C clusters, extrasynaptic and synaptic, the latter associated with glutamatergic synapses in dendritic spines. Both glutamatergic and GABAergic neurons expressed α1C in the soma and dendrites. In contrast to the N‐type channel GFP‐α1B, GFP‐α1C was excluded from distal axons and nerve terminals of mature neurons. In developing neurons, however, α1C and α1C‐HA were robustly expressed in the growth cone, indicating that specific targeting properties of neuronal compartments change during differentiation. Synaptic and extrasynaptic localizations of α1C correspond to putative roles of L‐type Ca2+ currents in synaptic modulation and in the propagation of dendritic Ca2+ spikes, respectively. The transiently expressed α1C in the growth cone may be involved in neurite extension and axonal pathfinding.
Survival, regeneration and functional recovery of motoneurons in adult rats by reimplantation of ventral root following spinal root avulsion
Authors: Gu Huai‐Yu , Chai Hong , Zhang Jian‐Yi , Yao Zhi‐Bin , Zhou Li‐Hua , Wong Wai‐Man , Bruce Iain , Wu Wu‐Tian 
Published: April 2004

AbstractWe investigated the functional recovery of motoneurons after reimplanting an avulsed ventral root in a rat model of traction injury. The eighth cervical root (C8) was avulsed by controlled traction and immediately reimplanted to the spinal cord. Spinal nerves from neighbouring segments (C5, C6, C7 and T1) were ligated and cut. After 12 or 20 weeks, the survival, regeneration and functional recovery of spinal motoneurons were evaluated by Nissl staining, retrograde labelling of motoneurons, NOS histochemistry, histological examination of muscle and nerve–muscle junction, electromyography and behavioural observation. In the control animals, about 14% or 11% of spinal motoneurons survived 12 or 20 weeks postinjury, respectively. By contrast, in animals with ventral root reimplantation, 62% and 55% of motoneurons survived at 12 or 20 weeks postinjury, respectively. Retrograde labelling and histological examination indicated that about 90% of the surviving motoneurons in the C8 segment regenerated axons into the reimplanted ventral root. Staining the muscles with silver and cholinesterase revealed new motor endplates in the reinnervated muscle. Functionally significant electromyographic responses in flexor digitorum superficialis and flexor carpi radialis were observed in experimental animals; however, the average latency of the motor action potentials was greater than normal control. The grasping test showed functional recovery of finger flexors and median nerve. In conclusion, our results indicate that spinal motoneurons can regenerate axons through reimplanted roots and reinnervate muscles to recover partial function.
Projections from the auditory cortex to the superior olivary complex in guinea pigs
Authors: Coomes Diana L. , Schofield Brett R. 
Published: April 2004

AbstractWe used anterograde tracing techniques to characterize projections from auditory cortex to the superior olivary complex (SOC) in guinea pigs. Large injections of fluorescent or biotinylated dextrans into the temporal cortex labeled many axons in the SOC. Labeled boutons were most numerous in the ventral nucleus of the trapezoid body, with additional boutons in all other olivary nuclei. The distribution of boutons was similar in the ipsilateral and contralateral SOC; however, the contralateral SOC had markedly fewer axons and boutons. Similar patterns of labeling were also observed following injections confined to primary auditory cortex or the dorsocaudal auditory field. Cortical axons in many of the SOC nuclei share numerous morphological features, suggesting that individual axons may innervate multiple nuclei and have widespread effects. In addition, some nuclei contain axons with branching or termination patterns unique to that nucleus; these axons may represent focused projections with effects limited to individual SOC nuclei. Given the many projections of SOC nuclei, cortico‐olivary projections are in a position to modify the activity of many brainstem auditory circuits.
Orexin‐A regulates growth hormone‐releasing hormone mRNA content in a nucleus‐specific manner and somatostatin mRNA content in a growth hormone‐dependent fashion in the rat hypothalamus
Authors: López Miguel , Seoane Luisa María , Tovar Sulay , Nogueiras Rubén , Diéguez Carlos , Señarís Rosa 
Published: April 2004

AbstractThe orexins or hypocretins are two neuropeptides involved in the regulation of diverse biological processes such as feeding, sleep and neuroendocrine function. Recent findings suggest a possible functional interaction between orexins, somatostatin and growth hormone‐releasing hormone (GHRH) in the rat hypothalamus. In order to understand the possible functional linkage between orexins and these neuropeptides, we determined the effects of intracerebroventricular orexin‐A administration on hypothalamic somatostatin and GHRH mRNA levels. Furthermore, we examined whether growth hormone (GH) mediates these interactions by using two animal models that showed GH deficiency: hypophysectomized rats and dwarf Lewis rats. Using in situ hybridization, our data showed that GHRH mRNA levels in the paraventricular nucleus of the hypothalamus are decreased after orexin‐A treatment, without changes in the arcuate nucleus of the hypothalamus. On the other hand, orexin‐A treatment induces a GH‐dependent stimulatory effect on somatostatin mRNA content in the periventricular nucleus of the hypothalamus. Finally, we demonstrated, for the first time, that hypophysectomized rats and dwarf Lewis rats, two classical models of GH deficiency with alterations in sleep patterns, showed a marked reduction in the GHRH mRNA levels in the paraventricular nucleus of the hypothalamus. These data improve our understanding of the interactions among the different systems involved in the control and pathophysiology of food intake, sleep and GH secretion.
Immunocytochemical localization of the α1A subunit of the P/Q‐type calcium channel in the rat cerebellum
Authors: Kulik Ákos , Nakadate Kazuhiko , Hagiwara Akari , Fukazawa Yugo , Luján Rafael , Saito Hiromitsu , Suzuki Noboru , Futatsugi Akira , Mikoshiba Katsuhiko , Frotscher Michael , Shigemoto Ryuichi 
Published: April 2004

AbstractAmong various types of low‐ and high‐threshold calcium channels, the high voltage‐activated P/Q‐type channel is the most abundant in the cerebellum. These P/Q‐type channels are involved in the regulation of neurotransmitter release and in the integration of dendritic inputs. We used an antibody specific for the α1A subunit of the P/Q‐type channel in quantitative pre‐embedding immunogold labelling combined with three‐dimensional reconstruction to reveal the subcellular distribution of pre‐ and postsynaptic P/Q‐type channels in the rat cerebellum. At the light microscopic level, immunoreactivity for the α1A protein was prevalent in the molecular layer, whereas immunostaining was moderate in the somata of Purkinje cells and weak in the granule cell layer. At the electron microscopic level, the most intense immunoreactivity for the α1A subunit was found in the presynaptic active zone of parallel fibre varicosities. The dendritic spines of Purkinje cells were also strongly labelled with the highest density of immunoparticles detected within 180 nm from the edge of the asymmetrical parallel fibre–Purkinje cell synapses. By contrast, the immunolabelling was sparse in climbing fibre varicosities and axon terminals of GABAergic cells, and weak and diffuse in dendritic shafts of Purkinje cells. The association of the α1A subunit with the glutamatergic parallel fibre–Purkinje cell synapses suggests that presynaptic channels have a major role in the mediation of excitatory neurotransmission, whereas postsynaptic channels are likely to be involved in depolarization‐induced generation of local calcium transients in Purkinje cells.
Accelerated accumulation of N‐ and C‐terminal βAPP fragments and delayed recovery of microtubule‐associated protein 1B expression following stroke in aged rats
Authors: Badan I. , Dinca I. , Buchhold B. , Suofu Y. , Walker L. , Gratz M. , Platt D. , Kessler CH. , Popa‐Wagner A. 
Published: April 2004

AbstractThe age‐related decline in plasticity of the brain may be one factor underlying poor functional recovery after stroke. In the present work we tested the hypothesis that the attenuation of neural plasticity in old age could be the result of an altered temporal relationship between factors promoting brain plasticity [microtubule‐associated protein 1B (MAP1B)] and neurotoxic factors such as C‐terminal βAPP. Focal cerebral ischemia was produced by reversible occlusion of the right middle cerebral artery in 3‐ and 20‐month‐old male Sprague‐Dawley rats. The functional outcome was assessed in neurobehavioral tests at 3, 7, 14 and 28 days after surgery. At the indicated timepoints, brains were removed and immunostained for C‐ and N‐terminal βAPP and MAP1B. At 2 weeks poststroke, we found an age‐related increase in the amount of the C‐terminal fragment of βAPP in the peri‐infarcted area and the infarct core as well as an early, vigorous incorporation of N‐terminal βAPP into the developing astroglial scar. The recovery of the plasticity‐associated protein MAP1B following stroke was delayed in both age groups and became prominent between days 14 and 28. As aged rats showed diminished functional recovery compared with young rats, these results suggest that the accumulation of C‐terminal βAPP, together with the early incorporation of N‐terminal βAPP into the glial scar, may over‐ride the beneficial role of plasticity factors such as MAP1B.
Age‐dependent expression of collapsin response mediator proteins (CRMPs) in cat visual cortex
Authors: Cnops Lieselotte , Van de Plas Babs , Arckens Lutgarde 
Published: April 2004

AbstractThe functional properties and anatomical organization of the mammalian visual cortex are immature at birth and develop gradually during the first postnatal weeks. There is a ‘critical period’ where the cortex is plastic and susceptible to changes in visual input. Knowledge of proteins with a high expression during this period has great importance for the understanding of activity‐driven maturation of the brain. The collapsin response mediator protein family consists of five cytosolic phosphoproteins (CRMP1–5) that are involved in neuronal differentiation during the development of the nervous system. They have been implicated in axon guidance and growth cone collapse through their action in the signalling pathway of collapsin/semaphorin. We examined the distribution of the CRMPs throughout the visual cortex of kitten and adult cat by in situ hybridization. While CRMP3 could not be detected in cat forebrain, the other CRMPs showed a higher expression in the immature brain compared to the adult state. Western blotting allowed the quantification of the observed age‐dependent differences in the expression of CRMP2, 4 and 5. Moreover, for CRMP2 and 5 we observed a number of development‐dependent post‐translational modifications. We thus conclude that CRMPs might be important during the normal postnatal development of the visual cortex possibly for the fine‐tuning of the specific connections in the brain.
Differential neuroplastic changes in neocortical movement representations and dendritic morphology in epilepsy‐prone and epilepsy‐resistant rat strains following high‐frequency stimulation
Authors: Flynn Corey , Monfils Marie‐H. , Kleim Jeffery A. , Kolb Bryan , McIntyre Dan C. , Campbell Teskey G. 
Published: April 2004

AbstractThe epileptogenic‐prone (FAST) and epileptogenic‐resistant (SLOW) rat strains have become a valuable tool for investigating the neurochemical and neurophysiological basis of epilepsy. This study examined the two strains with respect to their neocortical movement representations and cortical layer III pyramidal cell dendritic morphology in both control and potentiated conditions. FAST and SLOW rats received high‐frequency stimulation of the corpus callosum in order to induce long‐term polysynaptic potentiation of the transcallosal pathway to the sensorimotor neocortex. Baseline‐evoked potentials of this pathway were recorded in the left hemisphere before stimulation, and following 5, 10, 15 and 20 days of high‐frequency stimulation. All rats then underwent high‐resolution intracortical microstimulation (ICMS) in order to assess functional movement representations of the left caudal forelimb area of the sensorimotor cortex. Immediately following ICMS, the brains were stained with the Golgi–Cox method, and the length, branching and spine density of frontal and occipital neocortical layer III pyramidal neurons were measured. We observed that high‐frequency stimulation induced similar increases in polysynaptic potentiation in both rat strains; however, only the FAST strain showed an increase (doubling) in the size of their motor maps. We also observed decreases in dendritic length and branching in the FAST rats, and the opposite profile in the SLOW rats. The potentiated FAST rats also showed an increase in spine density. Our results suggest that differences in susceptibility to epileptogenesis may result in a differential response to stimulation‐induced plasticity.
Long‐term synaptic morphometry changes after induction of long‐term potentiation and long‐term depression in the dentate gyrus of awake rats are not simply mirror phenomena
Authors: Mezey Szilvia , Doyère Valérie , De Souza Ian , Harrison Elaine , Cambon Karine , Kendal Claire E. , Davies Heather , Laroche Serge , Stewart Michael G. 
Published: April 2004

AbstractMechanisms of expression of long‐term synaptic plasticity are believed to involve morphological changes of the activated synapses and remodelling of connectivity. Here, we investigated changes in synaptic and neuronal parameters in the dentate gyrus 24 h after induction of long‐term potentiation (LTP) and long‐term depression (LTD) in awake rats. In dentate granule cells, tetanization of the medial or lateral perforant paths induces LTP in specific synaptic bands along the dendrites in the middle and outer molecular layers, respectively, and tetanization of the lateral path induces robust LTD heterosynaptically in the middle molecular layer. This functional segregation allowed us to assess morphological changes associated with LTP and LTD in each pathway in the same population of neurons. Electron microscopy and unbiased counting methods were used to estimate neuronal density, axospinous, axodendritic and perforated synapse density, multiple synapse bouton density and postsynaptic density (PSD) area. Whereas there was no change in neuronal density, PSD area and multiple synapse boutons 24 h after either LTP or LTD, there was a noninput‐specific increase in unperforated axospinous synapses after both LTP and LTD. However, we found that LTP of the medial, but not lateral, perforant path is associated with a specific increase in perforated axospinous synapses in the potentiated area. We also show that heterosynaptic LTD is associated with an input‐specific increase in axodendritic synapse density. These results suggest that each perforant pathway may differ with respect to the nature of LTP‐induced long‐term changes and show that morphologically LTD is not simply the converse of LTP.
The delta agonists DPDPE and deltorphin II recruit predominantly mu receptors to produce thermal analgesia: a parallel study of mu, delta and combinatorial opioid receptor knockout mice
Authors: Scherrer Grégory , Befort Katia , Contet Candice , Becker Jérôme , Matifas Audrey , Kieffer Brigitte L. 
Published: April 2004

AbstractDelta‐selective agonists have been developed to produce potent analgesic compounds with limited side‐effects. DPDPE and deltorphin II are considered prototypes, but their delta‐selectivity in vivo and the true ability of delta receptors to produce analgesia remain to be demonstrated. Here we have performed a parallel analysis of mu, delta and combinatorial opioid receptor knockout mice, in which we found no obvious alteration of G‐protein coupling for remaining opioid receptors. We compared behavioural responses in two models of acute thermal pain following DPDPE and deltorphin II administration by intracerebroventricular route. In the tail‐immersion test, both compounds were fully analgesic in delta knockout mice and totally inactive in mu knockout mice. In the hotplate test, the two compounds again produced full analgesia in delta knockout mice. In mu knockout mice, there was significant, although much lower, analgesia. Furthermore, DPDPE analgesia in the delta knockout mice was fully reversed by the mu selective antagonist CTOP in both tests. Together, this suggests that mu rather than delta receptors are recruited by the two agonists for the tail withdrawal and the hotplate responses. Finally, deltorphin II slightly prolonged jump latencies in double mu/kappa knockout mice (delta receptors only) and this response was abolished in the triple knockout mice, demonstrating that the activation of delta receptors alone can produce weak but significant mu‐independent thermal antinociception.
Anxiety and Stress Responses in Female Oxytocin Deficient Mice
Authors: Amico J. A. , Mantella R. C. , Vollmer R. R. , Li X. 
Published: April 2004

AbstractOxytocin is believed to attenuate the response of the hypothalamic‐pituitary‐adrenal axis to stress and to be anxiolytic. Stressors with a psychological component evoke both central and peripheral secretion of oxytocin in laboratory rodents. Oxytocin gene deletion mice provide a novel way to understand the role of oxytocin in stress and anxiety‐related behaviours. We present our experience with female oxytocin deficient mice that were tested in an elevated plus maze (EPM), a behavioural test of anxiety, or exposed to psychogenic stressors (platform shaker or novel environment). Oxytocin‐deficient mice not only displayed more anxiety‐related behaviour, but also released more corticosterone after a psychogenic stressor and manifested greater stress‐induced hyperthermia compared to wild‐type mice. The diurnal variation of corticosterone and the response of corticosterone to corticotropin‐releasing factor were not significantly different between genotypes. We also measured Fos‐immunoreactive protein, an index of neuronal activation, in the medial amygdala of female mice after EPM testing. The medial amygdala is important for processing of psychogenic stress and anxiety and also contains oxytocin pathways and oxytocin receptors. The expression of Fos in the medial amygdala of mice not exposed to the EPM was not different between genotypes. Following EPM exposure, Fos expression was greater in oxytocin null compared to wild‐type mice. Our findings support the hypothesis that central oxytocin is anxiolytic, and attenuates the stress response to psychogenic provocation in female mice.
Oxytocin and Oxytocin Receptors in Cancer Cells and Proliferation
Authors: Cassoni P. , Sapino A. , Marrocco T. , Chini B. , Bussolati G. 
Published: April 2004

AbstractThe hypothalamic nonapeptide oxytocin plays a crucial role in many reproductive and behavioural functions. However, in recent years, an additional new role for oxytocin has been identified in neoplastic pathology. In tumours, oxytocin acts as a growth regulator, through the activation of a specific G‐coupled transmembrane receptor, the oxytocin receptor. In vitro, oxytocin inhibits proliferation of neoplastic cells of either epithelial (mammary and endometrial), nervous or bone origin, all expressing oxytocin receptor. Furthermore, an oxytocin growth‐inhibiting effect was also tested and confirmed in vivo in mouse and rat mammary carcinomas. In neoplastic cells derived from two additional oxytocin target tissues, trophoblast and endothelium, oxytocin was found to promote cell proliferation, an effect opposite to that previously described in all other neoplastic oxytocin‐responsive cells. The signal transduction pathways coupled to the biological effects of oxytocin are different in oxytocin growth‐inhibited or growth‐stimulated cells, and may depend on the membrane localization of the oxytocin receptor itself. The inhibitory effect of oxytocin is apparently mediated by activation of the cAMP‐protein kinase A pathway, a nonconventional oxytocin signalling pathway, whereas the mitogenic effect is coupled to the increase of intracellular [Ca2+] and tyrosine phosphorylation, ‘classical’ oxytocin transducers. Moreover, the oxytocin receptor localization in lipid rafts enriched in caveolin‐1 turns the inhibition of cell growth into a proliferative response, eliciting different epidermal growth factor receptor/mitogen‐activated protein kinase activation patterns. This unexpected role of oxytocin (and oxytocin analogues) in regulating cell proliferation, as well as the widespread expression of oxytocin receptors in neoplastic tissues of different origin, opens up new perspectives on the biological role of the oxytocin–oxytocin receptor system in cancer.