bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serotonin inhibits glutamate‐ but not PACAP‐induced per gene expression in the rat suprachiasmatic nucleus at night
Authors: Sanggaard K. M. , Hannibal J. , Fahrenkrug J. 
Published: December 2004

AbstractCircadian rhythms of physiology and behaviour generated by the brain's biological clock located in the suprachiasmatic nucleus are entrained by light via the retinohypothalamic tract. Two neurotransmitters, glutamate and pituitary adenylate cyclase‐activating polypeptide (PACAP), found in this monosynaptic pathway mediate the effects of light to the clock. It is well known that not only light entrains the clock. Nonphotic cues mediated by neurotransmitters such as serotonin reaching the suprachiasmatic nucleus from the midbrain raphe nucleus modulate light‐induced phase shifts at night. Two clock genes, per1 and per2, have been attributed a role in light‐induced phase shift. In the present study, using an in vitro brain slice model and quantitative in situ hybridization for per1 and per2, we have shown that serotonin induces per1 gene expression at late subjective night but not at early night. Furthermore, serotonin application before glutamate or PACAP blocked glutamate‐induced per1 expression at early night and per2 gene expression at late night. In contrast, serotonin did not influence PACAP‐induced per gene expression at late night. Triple antigen immunohistochemistry and confocal microscopy supported both a pre‐ and post‐synaptic interaction of retinohypothalamic tract (PACAP‐immunoreactive) and serotonin projections on vasoactive intestinal peptide‐ and gastrin‐releasing peptide‐containing cell bodies in the ventro‐lateral suprachiasmatic nucleus. Our findings suggest that the per genes could be the molecular target for the modulatory effects of serotonin on light signalling to the clock.
Altered hemispheric asymmetry of auditory P100m in dyslexia
Authors: Heim Sabine , Eulitz Carsten , Elbert Thomas 
Published: December 2004

AbstractIn various studies, deviances of hemispheric laterality in the organization of the perisylvian region in dyslexia have been suggested. Although associated with impaired language functioning, the clinical significance of atypical cerebral lateralization remains unclear. The present study examined interhemispheric source differences of magnetic responses to the German synthetic syllable [ba:] in the auditory cortex of 14 dyslexic children and 12 normally literate controls aged 8–15 years. In all subjects, two main deflections, P100m and N260m, were evident in the responses over each hemisphere. While in the control group the right P100m dipole was located more anterior than the corresponding dipole of the left hemisphere, the dyslexic group displayed a rather symmetrical source configuration between the hemispheres. This symmetry reflected a deviance in the right perisylvian region for the dyslexic subjects' P100m, which was generated ≈1 cm more posterior than the response in controls. The deviation was also obvious relative to the source location of the later component, N260m, which did not systematically differ between the participant groups. Our results suggest that the altered hemispheric asymmetry reflects an atypical organization of the right hemisphere in children and adolescents with dyslexia.
Potentiation of parkinsonian symptoms by depletion of locus coeruleus noradrenaline in 6‐hydroxydopamine‐induced partial degeneration of substantia nigra in rats
Authors: Srinivasan J. , Schmidt W. J. 
Published: December 2004

AbstractParkinson's disease is characterized not only by a progressive loss of dopaminergic neurons in the substantia nigra but also by a degeneration of locus coeruleus noradrenergic neurons. The present study addresses the question of whether a partial neurodegeneration of dopaminergic neurons using 6‐hydroxydopamine in rat, not sufficient to produce motor disturbances, is potentiated by prior selective denervation of locus coeruleus noradrenergic terminal fields using N‐ethyl‐2‐bromobenzylamine. Two types of denervations, one causing dopamine deficiency alone and the other causing noradrenaline and dopamine deficiency, were performed. Noradrenaline, 5‐hydroxytryptamine, 5‐hydroxyindole acetic acid, dopamine and its metabolites were analysed in various brain regions. Behaviour was evaluated by catalepsy tests and activity box. N‐ethyl‐2‐bromobenzylamine selectively depleted noradrenaline from neurons of locus coeruleus origin. Decreased dopamine content in the striatum, substantia nigra and pre‐frontal cortex was observed after dopaminergic lesion with 6‐hydroxydopamine (42.9%). Additional locus coeruleus noradrenaline depletion with N‐ethyl‐2‐bromobenzylamine aggravated the dopamine depletion (61.2%). The lesion in the noradrenergic and dopaminergic neurodegenerated group was not sufficient to induce consistent catalepsy and akinesia. However, after a subthreshold dose of haloperidol (0.1 mg/kg), the expression of catalepsy and akinesia was strong in the dual‐lesioned group and less in the 6‐hydroxydopamine‐lesioned group. These results indicate that denervation of locus coeruleus noradrenergic terminals with N‐ethyl‐2‐bromobenzylamine potentiates the 6‐hydroxydopamine‐induced partial dopaminergic neurodegeneration and parkinsonian symptoms. Based on the present findings and existing reports, it can be concluded that noradrenergic neurons of locus coeruleus have neuromodulatory and neuroprotective properties on the dopaminergic neurons of basal ganglia and that noradrenergic degeneration may contribute to the aetiology and pathophysiology of Parkinson's disease.
Long‐term potentiation in freely moving rats reveals asymmetries in thalamic and cortical inputs to the lateral amygdala
Authors: Doyère Valérie , Schafe Glenn E. , Sigurdsson Torfi , LeDoux Joseph E. 
Published: December 2004

AbstractLong‐term memory underlying Pavlovian fear conditioning is believed to involve plasticity at sensory input synapses in the lateral nucleus of the amygdala (LA). A useful physiological model for studying synaptic plasticity is long‐term potentiation (LTP). LTP in the LA has been studied only in vitro or in anaesthetized rats. Here, we tested whether LTP can be induced in auditory input pathways to the LA in awake rats, and if so, whether it persists over days. In chronically implanted rats, extracellular field potentials evoked in the LA by stimulation of the auditory thalamus and the auditory association cortex, using test simulations and input/output (I/O) curves, were compared in the same animals after tetanization of either pathway alone or after combined tetanization. For both pathways, LTP was input‐specific and long lasting. LTP at cortical inputs exhibited the largest change at early time points (24 h) but faded within 3 days. In contrast, LTP at thalamic inputs, though smaller initially than cortical LTP, remained stable until at least 6 days. Comparisons of I/O curves indicated that the two pathways may rely on different mechanisms for the maintenance of LTP and may benefit differently from their coactivation. This is the first report of LTP at sensory inputs to the LA in awake animals. The results reveal important characteristics of synaptic plasticity in neuronal circuits of fear memory that could not have been revealed with in vitro preparations, and suggest a differential role of thalamic and cortical auditory afferents in long‐term memory of fear conditioning.
Long‐term potentiation recruits a trisynaptic excitatory associative network within the mouse dentate gyrus
Authors: Kleschevnikov Alexander M. , Routtenberg Aryeh 
Published: December 2004

AbstractGranule cells of the hippocampal dentate gyrus receive two powerful excitatory inputs: the perforant path, originating from the entorhinal cortex, and the associational pathway, originating from mossy cells, the principal neurons of the dentate gyrus hilus. We examined the electrophysiological properties of the less well‐studied associational pathway and its interaction with the perforant path in the intact mouse hippocampus and then tested homosynaptic, trans‐synaptic and associative long‐term potentiation of these pathways. The associational pathway was either monosynaptically activated by stimulation within the inner molecular layer or trisynaptically activated after stimulation of the perforant path. Laminar profiles of extracellularly recorded associational pathway field potentials demonstrated a bell‐shaped curve with a peak in the inner molecular layer. Tetanization of the perforant path induced not only homosynaptic potentiation of the perforant path (162.4 ± 6.7% at 0.5–1.5 h after tetanus) but also heterosynaptic potentiation of the associational pathway (115.7 ± 4.9%). Direct tetanization of the associational pathway within the inner molecular layer was ineffective in either the septo‐temporal (97.2 ± 4.5%) or temporal‐septal (104.4 ± 4.6%) direction. In contrast, conjoint tetanization of the associational pathway with the perforant path potentiated the associational pathway responses in both the septo‐temporal (123.4 ± 5.8%) and the temporal‐septal (124.8 ± 7.3%) directions. Paired‐pulse facilitation was attenuated by long‐term potentiation in the perforant path and the associational pathway, suggesting pre‐synaptic involvement. These results demonstrate that long‐term potentiation of the associational pathway and the perforant path is a product of the network properties of the dentate gyrus rather than of each monosynaptic input alone. The architecture of this neural network may be designed for flexible dynamic associations of the afferent perforant path inputs to configure encoded information within hippocampal neuronal ensembles.
The role of CD36 in peripheral nerve remyelination after crush injury
Authors: Eto Masaki , Yoshikawa Hiroo , Fujimura Harutoshi , Naba Ichiro , Sumi‐Akamaru Hisae , Takayasu Satoshi , Itabe Hiroyuki , Sakoda Saburo 
Published: December 2004

AbstractWe previously demonstrated that the deficiency of class A macrophage scavenger receptor type I/II was involved in the delayed phagocytosis of degraded myelin by macrophages in class A macrophage scavenger receptor type I/II knockout mice after crush injury of the sciatic nerve [Naba et al. (2000) Exp. Neurol., 166, 83–89]. In order to elucidate the role of CD36, one of the scavenger receptors, here we inflicted crush injury to the sciatic nerves of CD36 knockout mice and investigated the remyelination after crush injury in comparison with that of class A macrophage scavenger receptor type I/II knockout mice. Although we previously reported a lot of onion‐bulbs in class A macrophage scavenger receptor type I/II knockout mice at 3 weeks, the number of onion‐bulbs was limited both in CD36 knockout mice and wild‐type mice. In the morphometry, the remyelination was seriously delayed, and the infiltrating macrophages into the nerve fascicles were quite frequent in CD36 knockout mice compared with wild‐type mice at 3 and 6 weeks postinjury. The immunohistochemistry with the monoclonal antibody reacted with oxidized phosphatidylcholine and oil red O staining were positive in wild‐type mice, but were negative in CD36 knockout mice, suggesting that the oxidation of phosphatidylcholine and the generation of neutral lipids in macrophages were disturbed in CD36 knockout mice. We hypothesize that the delayed phagocytosis by macrophages and the defect in reuse of lipids from degraded myelin are related to seriously delayed remyelination and a small number of onion‐bulbs in CD36 knockout mice.
Anterograde delivery of brain‐derived neurotrophic factor to striatum via nigral transduction of recombinant adeno‐associated virus increases neuronal death but promotes neurogenic response following stroke
Authors: Gustafsson Elin , Andsberg Gunnar , Darsalia Vladimer , Mohapel Paul , Mandel Ronald J. , Kirik Deniz , Lindvall Olle , Kokaia Zaal 
Published: December 2004

AbstractTo explore the role of brain‐derived neurotrophic factor for survival and generation of striatal neurons after stroke, recombinant adeno‐associated viral vectors carrying brain‐derived neurotrophic factor or green fluorescent protein genes were injected into right rat substantia nigra 4–5 weeks prior to 30 min ipsilateral of middle cerebral artery occlusion. The brain‐derived neurotrophic factor–recombinant adeno‐associated viral transduction markedly increased the production of brain‐derived neurotrophic factor protein by nigral cells. Brain‐derived neurotrophic factor was transported anterogradely to the striatum and released in biologically active form, as revealed by the hypertrophic response of striatal neuropeptide Y‐positive interneurons. Animals transduced with brain‐derived neurotrophic factor‐recombinant adeno‐associated virus also exhibited abnormalities in body posture and movements, including tilted body to the right, choreiform movements of left forelimb and head, and spontaneous, so‐called ‘barrel’ rotation along their long axis. The continuous delivery of brain‐derived neurotrophic factor had no effect on the survival of striatal projection neurons after stroke, but exaggerated the loss of cholinergic, and parvalbumin‐ and neuropeptide Y‐positive, γ‐aminobutyric acid‐ergic interneurons. The high brain‐derived neurotrophic factor levels in the animals subjected to stroke also gave rise to an increased number of striatal cells expressing doublecortin, a marker for migrating neuroblasts, and cells double‐labelled with the mitotic marker, 5‐bromo‐2′‐deoxyuridine‐5′monophosphate, and early neuronal (Hu) or striatal neuronal (Meis2) markers. Our findings indicate that long‐term anterograde delivery of high levels of brain‐derived neurotrophic factor increases the vulnerability of striatal interneurons to stroke‐induced damage. Concomitantly, brain‐derived neurotrophic factor potentiates the stroke‐induced neurogenic response, at least at early stages.
Distinct functions of Rac1 and Cdc42 during axon guidance and growth cone morphogenesis in Drosophila
Authors: Matsuura Ryouta , Tanaka Hideaki , Go Masahiro J. 
Published: December 2004

AbstractRho family small GTPases are thought to be key molecules in the regulation of cytoskeletal organization, especially for actin filaments. In order to examine the functions of Rac1 and Cdc42 in axon guidance at the midline of the central nervous system in Drosophila embryos, we either activated or inactivated Rac1 and Cdc42 in all postmitotic neurons. We found that the phenotypes of Cdc42 activation and Rac1 inactivation were similar to those of roundabout mutants, in that many extra axons crossed the midline. We also found that Rac1 inactivation is dominant over Roundabout receptor activation. Our observations indicate that Rac1 and Cdc42 have distinct functions in downstream signalling events triggered by Roundabout receptors. In order to further examine the functional difference between Rac1 and Cdc42 in the growth cone morphogenesis, we used primary embryonic cultures to closely observe neurite formation. We showed that activation of Rac1 and Cdc42 has distinct effects on neurite formation, particularly on growth cone morphology and the actin filaments within. Both Rac1 and Cdc42 activation induced large growth cones and long filopodia, but Cdc42 did so more efficiently than Rac1. Only Rac1 activation, however, induced thick actin bundles in the filopodia. We also found a clear difference between Rac1 and Cdc42 in terms of the response to an inhibitor of actin polymerization. Our results suggest that Cdc42 is specifically involved in the regulation of actin filaments in growth cones, whereas Rac1 is involved in additional functions.
Two oceans, two taxa and one mode of development: latitudinal diversity patterns of South American crabs and test for possible causal processes
Authors: Astorga Anna , Fernández Miriam , Boschi Enrique E. , Lagos Nelson 
Published: December 2004

AbstractThe latitudinal gradient of species diversity is a widely recognized but poorly understood phenomenon. In marine systems, differences in dispersal abilities among species may pose an additional problem in identifying the processes that affect diversity. We compared latitudinal diversity gradients along two parallel continental coasts, the east and west coasts of South America, of two groups of Crustacea (Brachyura and Anomura), which exclusively exhibit planktonic development. We also evaluated the species‐area and the energy‐input hypotheses. Diversity decreased with increasing latitude for both groups in both oceans. Results suggest that the spatial structure of sea surface temperature (SST) explains diversity of both groups at large, but not small (< 5°), scales. Range size and latitude were not correlated. We hypothesize that SST differentially affects taxa with contrasting modes of development, influencing patterns of diversity. We suggest that developmental modes of marine organisms should be considered in future diversity analyses.
Parameter drift stabilizes long‐range extinction forecasts
Authors: Halley J. M. 
Published: December 2004

AbstractEstimates of the reliability of population viability analysis (PVA), accounting for uncertainties in model parameters, often arrive at confidence intervals for extinction probability so wide as to be almost meaningless. This lack of precision is a consequence of extreme sensitivity to average linear growth rate, when predicting to a distant time horizon. Longer‐term trends or drift in parameter values (a form of ‘reddened’ environmental variability) will also affect the accuracy of such forecasts. This letter reports how, contrary to intuition, introducing such a component of variability may improve the precision of extinction forecasts. The paradoxical result arises because the dependence of extinction probability on growth rate is weakened, and shifted onto other parameters (e.g. diffusion strength) where dependence is less sensitive. This offers hope that, with reasonable knowledge of environmental stochasticity, it may still be meaningful to carry out longer range PVAs.
The role of host sex in parasite dynamics: field experiments on the yellow‐necked mouseApodemus flavicollis
Authors: Ferrari Nicola , Cattadori Isabella M. , Nespereira Javier , Rizzoli Annapaola , Hudson Peter J. 
Published: December 2004

AbstractWe investigated the role of host sex in parasite transmission and questioned: ‘Is host sex important in influencing the dynamics of infection in free living animal populations?’ We experimentally reduced the helminth community of either males or females in a yellow‐necked mice (Apodemus flavicollis) population using an anthelmintic, in replicated trapping areas, and subsequently monitored the prevalence and intensity of macroparasites in the untreated sex. We focussed on the dominant parasiteHeligmosomoides polygyrusand found that reducing parasites in males caused a consistent reduction of parasitic intensity in females, estimated through faecal egg counts, but the removal of parasites in females had no significant influence on the parasites in males. This finding suggests that males are responsible for driving the parasite infection in the host population and females may play a relatively trivial role. The possible mechanisms promoting such patterns are discussed.
Social life‐history response to individual immune challenge of workers of Bombus terrestris L.: a possible new cooperative phenomenon
Authors: Moret Yannick , Schmid‐Hempel Paul 
Published: December 2004

AbstractParasites typically reduce host survival or fecundity. To minimize fitness loss, hosts can make temporal adjustments of their reproductive effort. To date such plastic shifts of life‐history traits in response to parasitism are only known from solitary organisms where infected individuals can react by themselves. In the case of social insects, where brood care and reproductive effort is shared between reproductive individuals (typically the queen) and workers, adjustments of the reproductive effort would depend on collective decision‐making. We tested for this possibility by experimentally activating the immune response of individual workers in colonies of the bumblebee, Bombus terrestris L. This induction resulted, in combination with environmental conditions, in a reduction of fitness of the social unity (i.e. colony success, measured by number and biomass of offspring) and a collective response towards earlier reproduction. As both phenomena are expressed at the level of the colony, the result suggests that key elements of the use of immune defence have been maintained through the evolutionary transition to sociality.
Are viruses driving microbial diversification and diversity?
Authors: Weinbauer Markus G. , Rassoulzadegan Fereidoun 
Published: December 2004

SummaryViruses can influence the genetic diversity of prokaryotes in various ways. They can affect the community composition of prokaryotes by ‘killing the winner’ and keeping in check competitive dominants. This may sustain species richness and the amount of information encoded in genomes. Viruses can also transfer (viral and host) genes between species. Such mechanisms have probably influenced the speciation of prokaryotes. Whole‐genome sequencing has clearly revealed the importance of (virus‐mediated) gene transfer. However, its significance for the ecological performance of aquatic microbial communities is only poorly studied, although the few available reports indicate a large potential. Here, we present data supporting the hypothesis that viral genes and viral activity generate genetic variability of prokaryotes and are a driving force for ecological functioning and evolutionary change.
Functional gene diversity analysis in BTEX contaminated soils by means of PCR‐SSCP DNA fingerprinting: comparative diversity assessment against bacterial isolates and PCR‐DNA clone libraries
Authors: Junca Howard , Pieper Dietmar H. 
Published: December 2004

SummaryDevelopments in molecular biology based techniques have led to rapid and reliable tools to characterize microbial community structures and to monitor their dynamics under in situ conditions. However, there has been a distinct lack of emphasis on monitoring the functional diversity in the environment. Genes encoding catechol 2,3‐dioxygenases (C23O), as key enzymes of various aerobic aromatic degradation pathways, were used as functional targets to assess the catabolic gene diversity in differentially BTEX contaminated environments by polymerase chain reaction‐single‐strand conformation polymorphism (PCR‐SSCP). Site specific PCR‐SSCP fingerprints were obtained, showing that gene diversity experienced shifts correlated to temporal changes and levels of contamination. PCR‐SSCP enabled the recovery of predominant gene polymorphs, and results closely matched with the information retrieved from random sequencing of PCR‐DNA clone libraries. A new method for isolating strains capable of growing on BTEX compounds was developed to diminish preselection or enrichment bias and to assess the function of predominant gene polymorphs. C23O abundance in isolates correlated with the levels of BTEX pollution in the soil samples analysed. Isolates harbouring C23O genes, identical to the gene polymorph predominant in all contaminated sites analysed, showed an unexpected benzene but not toluene mineralizing phenotype whereas isolates harbouring a C23O gene variant differing by a single point mutation and observed in highly polluted sites only, were capable, among some other isolates, to mineralize benzene and toluene, indicating a catabolically determined sharing of carbon sources on‐site. The PCR‐SSCP technique is thus a powerful tool for assessing the diversity of functional genes and the identification of predominant gene polymorphs in environmental samples as a prerequisite to understand the functioning of microbial communities.