bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fertility Results of Artificial Inseminations Performed with Liquid Boar Semen Stored in X‐CellTM vs BTS Extender
Authors: Haugan T , Gaustad AH , Reksen O , Gröhn YT , Hofmo PO 
Published: September 2006

ContentsThe objective of the present field study was to compare the fertility results for boar semen diluted in X‐cellTM stored up to 4–5 days before artificial insemination (AI) with semen diluted in Beltsville thawing solution (BTS) used for AI following 2–3 days of storage (where the first day being the collection day). A total number of 2601 double inseminations in Norwegian herds were included in this two‐trial study. All the boars used in the study were mature cross‐bred Norwegian Landrace × Duroc (LD), which were routinely used for AI in Norway. The inseminated gilts and sows were Norwegian Landrace × Yorkshire (LY). The AI doses contained 2.5 billion spermatozoa, and consisted of a mixture of semen from three, occasionally four, boars (i.e. heterospermic semen). Fertility was measured in terms of the likelihood of farrowing and subsequent litter size. The fertility of the semen in both of the extenders was satisfactory and no significant differences were found either in semen stored 4–5 days in X‐cellTM compared with 2–3 days in BTS or in semen stored 2–3 days in X‐cellTM compared with 2–3 days in BTS. The storage capability findings for the long‐term extender X‐cellTM could significantly simplify the practical issues of semen production and the distribution of AI doses containing 2.5 billion spermatozoa. However, in pig production systems where all semen is used within 2–3 days, the short‐term extender BTS is as good as the more expensive extender X‐cellTM.
Ryanodine receptor–transmitter release site coupling increases quantal size in a synapse‐specific manner
Authors: Dunn Tyler W. , Syed Naweed I. 
Published: September 2006

AbstractThe mechanisms by which presynaptic neurones differentially regulate synaptic transmission with multiple postsynaptic targets in the brain are not fully understood. Using intracellular sharp electrode and whole‐cell voltage‐clamp recordings of soma–soma synapses between identifiedLymnaeaneurones, we provide direct evidence that quantal size is regulated presynaptically through the coupling of multiple release sites. This coupling effectively multiplies quantal size, thereby providing significant influence over parameters of synaptic transmission that are influenced by quantal size, such as the variance in transmitter release at stationary release probabilities. Variation in the degree of coupling is dependent on the identity of the postsynaptic cell, even though the variation in quantal size is of presynaptic origin. We have therefore demonstrated the presence of a novel mechanism by which presynaptic neurones may differentially regulate quantal size at select synaptic connections, in turn providing them with a means of regulating synaptic transmission with multiple postsynaptic cells.
The axotomy‐induced neuropeptides galanin and pituitary adenylate cyclase‐activating peptide promote axonal sprouting of primary afferent and cranial motor neurones
Authors: Suarez Victor , Guntinas‐Lichius Orlando , Streppel Michael , Ingorokva Shota , Grosheva Maria , Neiss Wolfram F. , Angelov Doychin N. , Klimaschewski Lars 
Published: September 2006

AbstractThe neuropeptides galanin and pituitary adenylate cyclase‐activating peptide (PACAP) are markedly up‐regulated in response to peripheral nerve lesion. Both peptides are involved in neuronal differentiation and neurite outgrowth during development. In this study, we investigated the effects of galanin and PACAP on axonal elongation and sprouting by adult rat sensory neurones in vitro and facial motor neurones in vivo. Dissociated rat dorsal root ganglion neurones were plated on laminin substrate and analysed morphometrically. Both the mean axonal length and the number of branch points significantly increased in the presence of galanin or PACAP (2–5 µm). Effects on axonal collateralization were investigated in the rat facial nerve lesion model by direct application of the peptides to collagen‐filled conduits entubulating the transected facial nerve stumps. Triple retrograde labelling of brainstem neurones confirmed that the peptides potently induce axonal sprouting of cranial motor neurones. The number of neurones regenerating into identified rami of the facial nerve increased up to fivefold. Biometrical analysis of whisking behaviour revealed that galanin and PACAP impaired the functional outcome when compared with vehicle‐treated animals 8 weeks after surgery. In conclusion, although galanin and PACAP have been established as neurotrophic molecules with respect to axonal development and regeneration, their potential as treatments for peripheral nerve lesions appears limited because of the extensive stimulation of collateral axon branching. These branches are misrouted towards incorrect muscles and cause impairment in their coordinated activity.
Brain‐derived neurotrophic factor facilitates in vivo internalization of tetanus neurotoxin C‐terminal fragment fusion proteins in mature mouse motor nerve terminals
Authors: Roux Sylvie , Saint Cloment Cécile , Curie Thomas , Girard Emmanuelle , Mena Francisco‐Javier Miana , Barbier Julien , Osta Rosario , Molgó Jordi , Brûlet Philippe 
Published: September 2006

AbstractIn a previous study it was reported that fusion proteins composed of the atoxic C‐terminal fragment of tetanus toxin (TTC) and green fluorescent protein or β‐galactosidase (GFP‐TTC and β‐gal‐TTC, respectively) rapidly cluster at motor nerve terminals of the mouse neuromuscular junction (NMJ). Because this traffic involves presynaptic activity, probably via the secretion of active molecules, we examined whether it is affected by brain‐derived neurotrophic factor (BDNF). Quantitative confocal microscopy and a fluorimetric assay for β‐gal activity revealed that co‐injecting BDNF and the fusion proteins significantly increased the kinetics and amount of the proteins' localization at the NMJ and their internalization by motor nerve terminals. The observed increases were independent of synaptic vesicle recycling because BDNF did not affect spontaneous quantal acetylcholine release. In addition, injecting anti‐BDNF antibody shortly before injecting GFP‐TTC, and before co‐injecting GFP‐TTC and BDNF, significantly reduced the fusion protein's localization at the NMJ. Co‐injecting GFP‐TTC with neurotrophin‐4 (NT‐4) or glial‐derived neurotrophic factor (GDNF), but not with nerve growth factor, neurotrophin‐3 or ciliary neurotrophic factor, also significantly increased the fusion protein's localization at the NMJ. Thus, TTC probes may use for their neuronal internalization endocytic pathways normally stimulated by BDNF, NT‐4 and GDNF binding. Different tyrosine kinase receptors with similar signalling pathways are activated by BDNF/NT‐4 and GDNF binding. Thus, activated components of these signalling pathways may be involved in the TTC probes' internalization, perhaps by facilitating localization of receptors of TTC in specific membrane microdomains or by recruiting various factors needed for internalization of TTC.
Marked alterations in the gait timing and rhythmicity of patients withde novoParkinson's disease
Authors: Baltadjieva Rossitza , Giladi Nir , Gruendlinger Leor , Peretz Chava , Hausdorff Jeffrey M. 
Published: September 2006

AbstractLittle is known about the gait characteristics of subjects withde novoParkinson's disease (PD). We hypothesized that alterations in the spatio‐temporal characteristics of gait will already be quantifiable in these patients. The gait of 35 patients with idiopathic PD (mean age 60 years) who were in the early stages of the disease (Hoehn and Yahr stage 1.8 ± 0.5, median 2.0, range 1.0–2.5) and were not yet treated with any anti‐parkinsonian medications were compared with the gait of age‐ and sex‐matched healthy controls (n = 22). The patients walked more slowly and with reduced swing times while also exhibiting increased left/right swing asymmetry and marked inconsistencies in the timing of gait. By contrast, significant group differences in the peak forces at heel‐strike and in the stride‐to‐stride variability of the ground reaction forces (a reflection of muscle output consistency) were not observed. These findings indicate that inde novoPD, an altered gait pattern is observed, even though dramatic changes in the gait pattern may not yet be apparent visually (e.g. fairly intact gait speed). Furthermore, the results demonstrate that the observed alterations are not just side‐effects of treatments or complications of the disease. Instead, there is evidence for motor programming deficits in gait, as revealed by increased gait variability and asymmetry in timing. PD apparently impinges on the regulation of a consistent gait rhythm, even early in the course of the disease when observed alterations are not the result of any pharmacologic treatment.
Insulin‐like growth factor binding proteins: regulation in chronic active plaques in multiple sclerosis and functional analysis of glial cells
Authors: Chesik Daniel , De Keyser Jacques , Glazenburg Lisa , Wilczak Nadine 
Published: September 2006

AbstractStudies in experimental allergic encephalomyelitis, an animal model of multiple sclerosis (MS), suggest that astrocyte‐secreted insulin‐like growth factor binding protein‐2 (IGFBP‐2) helps target IGF‐1 to IGF‐1 receptor‐expressing oligodendrocytes and promote remyelination. We examined the presence of IGFBPs 1–6 in astrocytes in normal post‐mortem human brain tissue and lesions of MS by means of immunohistochemistry. Under normal conditions all six IGFBPs were detected. Compared to controls, hypertrophic astrocytes at the borders of chronic active MS lesions displayed increased immunoreactivity for IGFBP‐2 and IGFBP‐4. In vitro studies were performed to analyse the effects of IGFBPs on cellular proliferation of neonatal rat glial cells. Treatment of astrocytes with IGF‐1 and ‐2 enhanced proliferation whereas IGFBP‐2 and ‐4 inhibited cellular growth. Interestingly, combined treatment with IGFBP‐2 and IGF‐1 potentiated effects on cellular proliferation whereas combined treatment with IGFBP‐2 and IGF‐2 inhibited growth. Unlike IGFBP‐2, IGFBP‐4 inhibited proliferation in combined treatment with IGF‐1. In contrast, combined treatment with IGFBP‐2 and IGF‐1 resulted in decreased cell survival of oligodendrocyte precursor cells. Our results suggest that the up‐regulation of IGFBP‐2 in reactive astrocytes in MS lesions may primarily serve to enhance the IGF‐1‐mediated mitogenic stimulus for astrocytes rather than supporting oligodendrocyte survival.
The importance of the rat hippocampus for learning the structure of visual arrays
Authors: Sanderson David J. , Pearce John M. , Kyd Rachel J. , Aggleton John P. 
Published: September 2006

AbstractIt has been assumed that the integrity of the rodent hippocampus is required for learning the spatial distribution of visual elements in an array. Formally assessing this assumption is, however, far from straightforward as standard tests are amenable to alternative strategies. In order to provide a stringent test of this ability rats were trained on three concurrent visual discriminations in a water tank in which the stimuli in each pair of discriminations contained exactly the same elements but they differed in their spatial arrangement e.g. A|B vs. its mirror image B|A. Such ‘structural’ discriminations are a specific subtype of ‘configural’ or ‘nonlinear’ tasks. Following acquisition half of the rats received hippocampal lesions and all rats were retrained on the structural discriminations. Hippocampal lesions impaired the ability to relearn these ‘structural’ discriminations. In contrast, two other groups of rats with similar hippocampal lesions showed no impairment on relearning two non‐structural, configural discriminations: transverse patterning and biconditional learning. All three tasks used the same apparatus, the same stimulus elements, and similar training regimes. Superior performance by the rats with hippocampal lesions during a generalization decrement probe showed that hippocampal lesions had diminished sensitivity to ‘structural’ features on the biconditional task. While the rat hippocampus need not be required for all configural learning, it is important for the special case when the spatial arrangements of the elements are critical. This ability may be a prerequisite for the creation of mental snapshots, which underlie episodic memory.
Animal models of migraine: looking at the component parts of a complex disorder
Authors: Bergerot A. , Holland P. R. , Akerman S. , Bartsch T. , Ahn A. H. , MaassenVanDenBrink A. , Reuter U. , Tassorelli C. , Schoenen J. , Mitsikostas D. D. , Van Den Maagdenberg A. M. J. M. , Goadsby P. J. 
Published: September 2006

AbstractAnimal models of human disease have been extremely helpful both in advancing the understanding of brain disorders and in developing new therapeutic approaches. Models for studying headache mechanisms, particularly those directed at migraine, have been developed and exploited efficiently in the last decade, leading to better understanding of the potential mechanisms of the disorder and of the action for antimigraine treatments. Model systems employed have focused on the pain‐producing cranial structures, the large vessels and dura mater, in order to provide reproducible physiological measures that could be subject to pharmacological exploration. A wide range of methods using both in vivo and in vitro approaches are now employed; these range from manipulation of the mouse genome in order to produce animals with human disease‐producing mutations, through sensitive immunohistochemical methods to vascular, neurovascular and electrophysiological studies. No one model system in experimental animals can explain all the features of migraine; however, the systems available have begun to offer ways to dissect migraine's component parts to allow a better understanding of the problem and the development of new treatment strategies.
Targeted transgene expression in neuronal precursors: watching young neurons in the old brain
Authors: Couillard‐Despres Sebastien , Winner Beate , Karl Claudia , Lindemann Gudrun , Schmid Peter , Aigner Robert , Laemke Joern , Bogdahn Ulrich , Winkler Juergen , Bischofberger Josef , Aigner Ludwig 
Published: September 2006

AbstractProgress in the field of neurogenesis is limited by the lack of animal models allowing direct detection and analysis of living cells participating in neurogenesis. We engineered a transgenic mouse model that expresses the fluorescent reporter proteins enhanced green fluorescent protein or Discoma sp. reef coral red fluorescent protein under the control of the doublecortin (DCX) promoter, a gene specifically and transiently active in neuronal precursors and young neurons. The expression of the reporter proteins correlated with expression of the endogenous DCX protein, and with developmental and adult neurogenesis. Neurogenesis was unaffected by the presence of the fluorescent proteins. The transgenic mice allowed direct identification of the very few newly generated neurons present in the aged brain. We performed electrophysiological analysis and established that newly generated hippocampal granule cells in aged and young mice shared identical physiological properties. Hence, although the rate of neurogenesis tapers with ageing, a population of highly excitable young neurons indistinguishable to those found in younger animals is continuously generated. Therefore, maintenance of the fundamental properties of neuronal precursors even at advanced age suggests that stimulation of neurogenesis may constitute a valid strategy to counteract age‐related neuronal loss and cognitive declines.
Modulation of p75NTR‐dependent motor neuron death by a small non‐peptidyl mimetic of the neurotrophin loop 1 domain
Authors: Pehar Mariana , Cassina Patricia , Vargas Marcelo R. , Xie Youmei , Beckman Joseph S. , Massa Stephen M. , Longo Frank M. , Barbeito Luis 
Published: September 2006

AbstractThe p75 neurotrophin receptor (p75NTR) is expressed by degenerating spinal motor neurons in amyotrophic lateral sclerosis (ALS). The mature and pro‐form of nerve growth factor (NGF) activate p75NTR to trigger motor neuron apoptosis. However, attempts to modulate p75NTR‐mediated neuronal death in ALS models by downregulating or antagonizing p75NTR with synthetic peptides have led to only modest results. Recently, a novel ligand of p75NTR, compound LM11A‐24, has been identified. It is a non‐peptidyl mimetic of the neurotrophin loop 1 domain that promotes hippocampal neuron survival through p75NTR and exerts protection against p75NTR‐mediated apoptosis of oligodendrocytes induced by proNGF. Thus, LM11A‐24 appears to activate p75NTR‐linked survival but not death mechanisms, and may interfere with the ability of neurotrophins to induce apoptosis. Given these findings, we hypothesized that LM11A‐24 might be a particularly potent inhibitor of motor neuron degeneration. We examined the effects of LM11A‐24 on apoptosis of cultured rat embryonic motor neurons. Interestingly, in contrast to the effects observed in hippocampal cultures, LM11A‐24 was unable to prevent motor neuron apoptosis induced by trophic factor deprivation. However, picomolar concentrations of LM11A‐24 prevented p75NTR‐dependent motor neuron death induced by either exogenous addition of NGF or spinal cord extracts from symptomatic superoxide dismutase‐1G93A mice, in the presence of low steady‐state concentrations of nitric oxide. LM11A‐24 also inhibited motor neuron death induced by NGF‐producing reactive astrocytes in co‐culture conditions. These studies suggest that modulation of p75NTR by small molecule ligands targeting this receptor might constitute a novel strategy for preventing motor neuron degeneration.
Neurokinin3receptor antagonism attenuates cocaine's behavioural activating effects yet potentiates its dopamine‐enhancing action in the nucleus accumbens core
Authors: Jocham Gerhard , Lezoch Katharina , Müller Christian P. , Kart‐Teke Emriye , Huston Joseph P. , De Souza Silva M. Angélica 
Published: September 2006

AbstractSeveral lines of evidence indicate a role for neurokinin3receptors (NK3‐Rs) in behavioural activation and mechanisms governing reinforcement processes. In this study we investigated the effect of pretreatment with the NK3‐R antagonist, SR142801, (0.2 and 2.0 mg/kg) on the cocaine‐induced (10.0 mg/kg i.p.) increase in extracellular dopaminergic activity in the nucleus accumbens (NAc).In vivomicrodialysis in the NAc of freely moving rats showed that cocaine increased concentrations of dopamine (DA) to ∼350% in the core and ∼450% in the shell. Pre‐treatment with SR142801 significantly potentiated this effect in the core (to ∼550%), whereas this effect was not found in the shell. We also investigated the effects of NK3‐Rs antagonism on cocaine‐induced hyperactivity and conditioned place preference. SR142801 blocked the hyperactivity, but neither the conditioned place preference nor the conditioned locomotor activity induced by cocaine, although there was a slight tendency towards a reduced place preference. When given alone, SR142801 had no effects on behaviour or extracellular dopamine concentrations in any of the structures investigated. These data provide evidence for a contribution of NK3‐Rs in the acute behavioural and neurochemical effects of cocaine, involving dopaminergic activity in the core of the nucleus accumbens.
Changes in extracellular hypothalamic glucose in relation to feeding
Authors: Mayer C. H. , Fink H. , Rex A. , Voigt J. ‐P. 
Published: September 2006

AbstractThe aim of the present in vivo microdialysis study was to investigate the relation between feeding and changes in glucose concentrations in the rat ventromedial hypothalamus (VMH). Absolute ambient glucose concentrations in VMH were 1.43 mm in non‐deprived rats as compared to 0.94 mm after 24‐h food deprivation. To examine whether feeding influences hypothalamic glucose, changes of glucose concentration over time were determined relative to a baseline. Experiments were conducted in relation to both, nutritional state (food‐deprived rats vs. non‐deprived rats) and feeding conditions throughout the experiment (freely feeding rats vs. rats without access to food). The results of this microdialysis study show clearly that glucose concentration in the VMH of rats increases significantly in relation to food intake. The data demonstrate that a 24‐h food deprivation before the experiment further augments this increase (up to 350% from baseline) as compared to non‐deprived conditions (up to 60% from baseline). However, the magnitude of food related increase in VMH glucose does not correlate with the individual amount of food eaten. In conclusion, the present study shows for the first time that VMH glucose concentrations increase with food intake in the early dark phase, indicating that such changes do not only occur after pharmacological treatment, but also under physiological feeding conditions. The results further indicate that the feeding related increase in VMH glucose depends on the nutritional state of the organism.
Chronic high‐frequency stimulation of the subthalamic nucleus and L‐DOPA treatment in experimental parkinsonism: effects on motor behaviour and striatal glutamate transmission
Authors: Gubellini Paolo , Eusebio Alexandre , Oueslati Abid , Melon Christophe , Kerkerian‐Le Goff Lydia , Salin Pascal 
Published: September 2006

AbstractHyperactivity of striatal glutamatergic synaptic transmission in response to dopamine depletion plays a major role in the pathogenesis of parkinsonian motor symptoms. In the present study we investigated the impact, on this hyperactivity, of chronic dyskinesiogenic L‐DOPA treatment, combined or not with high‐frequency stimulation (HFS) of the subthalamic nucleus (STN).In vitropatch‐clamp recordings were performed from striatal spiny neurons of hemiparkinsonian rats (intranigral 6‐OHDA injection). Here we show that dyskinesiogenic L‐DOPA treatment exacerbated striatal glutamatergic hyperactivity induced by 6‐OHDA lesion. Chronic 5‐day STN HFS had the opposite effect, reducing striatal glutamatergic transmission in both parkinsonian and dyskinetic animals. Consistently, chronic HFS stimulation could progressively ameliorate motor parkinsonian signs (akinesia) but, conversely, did not improve L‐DOPA‐induced dyskinesia (LID). Thus, the effects of L‐DOPA and HFS on corticostriatal transmission seem to be dissociated. These data show for the first time that dyskinesiogenic L‐DOPA treatment and chronic STN HFS with antiakinetic effects induce opposite plastic rearrangements in the striatum. The interaction between these two treatments provides further evidence that striatal glutamatergic hyperactivity is a pathophysiological correlate of akinesia rather than LID.