bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Optimization of Rural Landscape in the Light of the Idea of Sustainable Development – The Example of Poland
Authors: Sobala Michał , Myga-Piątek Urszula 
Published: October 2016

AbstractContemporary rural landscapes in Poland are being changed intensively and adversely. These changes lead to landscape disharmony, spatial disorder, the blurring of individual and specific features and disruption to the ecological equilibrium. This article aims to present general rules for the optimization of rural landscapes. It discusses the causes and consequences of unfavourable changes within Poland’s rural landscapes which constitute a threat to their sustainable development. The authors attempt to identify the major factors to be considered in taking steps aimed at landscape optimization. Landscape equilibrium may be assessed through the sustainable development dimensions: ethical, ecological, social, economic, technical, political and legal. Landscape optimization consists in maintaining the balance within these dimensions.
GIS-based Approach to Estimate Surface Runoff in Small Catchments: A Case Study
Authors: Vojtek Matej , Vojteková Jana 
Published: October 2016

AbstractThe issue of surface runoff assessment is one of the important and relevant topics of hydrological as well as geographical research. The aim of the paper is therefore to estimate and assess surface runoff on the example of Vyčoma catchment which is located in the Western Slovakia. For this purpose, SCS runoff curve number method, modeling in GIS and remote sensing were used. An important task was the creation of a digital elevation model (DEM), which enters the surface runoff modeling and affects its accuracy. Great attention was paid to the spatial interpretation of land use categories applying aerial imagery from 2013 and hydrological soil groups as well as calculation of maximum daily rainfall with N-year return periods as partial tasks in estimating surface runoff. From the methodological point of view, the importance of the paper can be seen in the use of a simple GIS-based approach to assess the surface runoff conditions in a small catchment.
Studying of the Nucleus-Nucleus Interaction Using Wave Function of the Nucleus and Hyperspherical Formalism
Authors: Pakdel Fatemeh , Rajabi Ali Akbar 
Published: October 2016

Abstract
The current study presents the results of the use of the wave function of a nucleus in place of the nucleus density distribution to calculate the nucleus-nucleus interaction potential. The wave function is obtained by solving the D-dimensional wave equation using the hyperspherical formalism. The interaction potential between two nuclei is calculated using the double folding model. The numerical results for the interaction potential and the scattering cross section are presented to evaluate the formalism used to calculate the nucleus wave function.
In UteroExposure to Valproic Acid Induces Neocortical Dysgenesis via Dysregulation of Neural Progenitor Cell Proliferation/Differentiation
Authors: Fujimura Kimino , Mitsuhashi Takayuki , Shibata Shinsuke , Shimozato Sachiko , Takahashi Takao 
Published: October 2016

Valproic acid (VPA), a widely used antiepileptic drug, is an inhibitor of histone deacetylases, which epigenetically modify cell proliferation/differentiation in developing tissues. A series of recent clinical studies in humans reported that VPA exposurein uteroimpaired histogenesis and the development of the central nervous system, leading to increased risks of congenital malformation and the impairment of higher brain functions in children. In the present study conducted in mice, we report that VPA exposurein utero(1) increases the amount of acetylated histone proteins, (2) alters the expression of G1-phase regulatory proteins, (3) inhibits the cell cycle exit of neural progenitor cells during the early stage of neocortical histogenesis, and (4) increases the production of projection neurons distributed in the superficial neocortical layers in embryonic brains. Together, our findings show that VPA exposurein uteroalters proliferation/differentiation characteristics of neural progenitor cells and hence leads to the neocortical dysgenesis.SIGNIFICANCE STATEMENTThis study provides new insight into the mechanisms of how an alteredin uteroenvironment, such as drug exposure, affects the generation of neurons prenatally. The antiepileptic drug valproic acid (VPA) is a good target molecule asin uteroexposure to VPA has been repeatedly reported to increase the risk of nervous system malformations and to impair higher brain functions in children. We show that VPA decreases the probability of differentiation of the neural progenitor cells (NPCs) in mice, resulting in an abnormally increased number of projection neurons in the superficial layers of the neocortex. Further, we suggest that histone deacetylase inhibition by VPA may be involved in the dysregulation of proliferation/differentiation characteristics of NPCs.
Fatigue in Rapsyn-Deficient Zebrafish Reflects Defective Transmitter Release
Authors: Wen Hua , Hubbard Jeffrey Michael , Wang Wei-Chun , Brehm Paul 
Published: October 2016

Rapsyn-deficient myasthenic syndrome is characterized by a weakness in voluntary muscle contraction, a direct consequence of greatly reduced synaptic responses that result from poorly clustered acetylcholine receptors. As with other myasthenic syndromes, the general muscle weakness is also accompanied by use-dependent fatigue. Here, we used paired motor neuron target muscle patch-clamp recordings from a rapsyn-deficient mutant line of zebrafish to explore for the first time the mechanisms causal to fatigue. We find that synaptic responses in mutant fish can follow faithfully low-frequency stimuli despite the reduced amplitude. This is in part helped by a compensatory increase in the number of presynaptic release sites in the mutant fish. In response to high-frequency stimulation, both wild-type and mutant neuromuscular junctions depress to steady-state response levels, but the latter shows exaggerated depression. Analysis of the steady-state transmission revealed that vesicle reloading and release at individual release sites is significantly slower in mutant fish during high-frequency activities. Therefore, reductions in postsynaptic receptor density and compromised presynaptic release collectively serve to reduce synaptic strength to levels that fall below the threshold for muscle action potential generation, thus accounting for use-dependent fatigue. Our findings raise the possibility that defects in motor neuron function may also be at play in other myasthenic syndromes that have been mapped to mutations in muscle-specific proteins.SIGNIFICANCE STATEMENTUse-dependent fatigue accompanies many neuromuscular myasthenic syndromes, including muscle rapsyn deficiency. Here, using a rapsyn-deficient line of zebrafish, we performed paired motor neuron target muscle patch-clamp recordings to investigate the mechanisms causal to this phenomenon. Our findings indicate that the reduced postsynaptic receptor density resulting from defective rapsyn contributes to weakness, but is not solely responsible for use-dependent fatigue. Instead, we find unexpected involvement of altered transmitter release from the motor neuron. Specifically, slowed reloading of vesicle release sites leads to augmented synaptic depression during repeated action potentials. Even at moderate stimulus frequencies, the depression levels for evoked synaptic responses fall below the threshold for the generation of muscle action potentials. The associated contraction failures are manifest as use-dependent fatigue.
A Functional Switch in Tonic GABA Currents Alters the Output of Central Amygdala Corticotropin Releasing Factor Receptor-1 Neurons Following Chronic Ethanol Exposure
Authors: Herman Melissa A. , Contet Candice , Roberto Marisa 
Published: October 2016

The corticotropin releasing factor (CRF) system in the central amygdala (CeA) has been implicated in the effects of acute ethanol and the development of alcohol dependence. We previously demonstrated that CRF receptor 1 (CRF1) neurons comprise a specific component of the CeA microcircuitry that is selectively engaged by acute ethanol. To investigate the impact of chronic ethanol exposure on inhibitory signaling in CRF1+ CeA neurons, we used CRF1:GFP mice subjected to chronic intermittent ethanol (CIE) inhalation and examined changes in local inhibitory control, the effects of acute ethanol, and the output of these neurons from the CeA. Following CIE, CRF1+ neurons displayed decreased phasic inhibition and a complete loss of tonic inhibition that persisted into withdrawal. CRF1− neurons showed a cell type-specific upregulation of both phasic and tonic signaling with CIE, the latter of which persists into withdrawal and is likely mediated by δ subunit-containing GABAAreceptors. The loss of tonic inhibition with CIE was seen in CRF1+ and CRF1− neurons that project out of the CeA and into the bed nucleus of the stria terminalis. CRF1+ projection neurons displayed an increased baseline firing rate and loss of sensitivity to acute ethanol following CIE. These data demonstrate that chronic ethanol exposure produces profound and long-lasting changes in local inhibitory control of the CeA, resulting in an increase in the output of the CeA and the CRF1 receptor system, in particular. These cellular changes could underlie the behavioral manifestations of alcohol dependence and potentially contribute to the pathology of addiction.SIGNIFICANCE STATEMENTThe corticotropin releasing factor (CRF) system in the central amygdala (CeA) has been implicated in the effects of acute and chronic ethanol. We showed previously that CRF receptor 1-expressing (CRF1+) neurons in the CeA are under tonic inhibitory control and are differentially regulated by acute ethanol (Herman et al., 2013). Here we show that the inhibitory control of CRF1+ CeA neurons is lost with chronic ethanol exposure, likely by a functional switch in local tonic signaling. The loss of tonic inhibition is seen in CRF1+ projection neurons, suggesting that a critical consequence of chronic ethanol exposure is an increase in the output of the CeA CRF1 system, a neuroadaptation that may contribute to the behavioral consequences of alcohol dependence.
Involvement of the Serotonin Transporter Gene in Accurate Subcortical Speech Encoding
Authors: Selinger Lenka , Zarnowiec Katarzyna , Via Marc , Clemente Immaculada C. , Escera Carles 
Published: October 2016

A flourishing line of evidence has highlighted the encoding of speech sounds in the subcortical auditory system as being shaped by acoustic, linguistic, and musical experience and training. And while the heritability of auditory speech as well as nonspeech processing has been suggested, the genetic determinants of subcortical speech processing have not yet been uncovered. Here, we postulated that the serotonin transporter-linked polymorphic region (5-HTTLPR), a common functional polymorphism located in the promoter region of the serotonin transporter gene (SLC6A4), is implicated in speech encoding in the human subcortical auditory pathway. Serotonin has been shown as essential for modulating the brain response to sound both cortically and subcortically, yet the genetic factors regulating this modulation regarding speech sounds have not been disclosed. We recorded the frequency following response, a biomarker of the neural tracking of speech sounds in the subcortical auditory pathway, and cortical evoked potentials in 58 participants elicited to the syllable /ba/, which was presented >2000 times. Participants with low serotonin transporter expression had higher signal-to-noise ratios as well as a higher pitch strength representation of the periodic part of the syllable than participants with medium to high expression, possibly by tuning synaptic activity to the stimulus features and hence a more efficient suppression of noise. These results imply the 5-HTTLPR in subcortical auditory speech encoding and add an important, genetically determined layer to the factors shaping the human subcortical response to speech sounds.SIGNIFICANCE STATEMENTThe accurate encoding of speech sounds in the subcortical auditory nervous system is of paramount relevance for human communication, and it has been shown to be altered in different disorders of speech and auditory processing. Importantly, this encoding is plastic and can therefore be enhanced by language and music experience. Whether genetic factors play a role in speech encoding at the subcortical level remains unresolved. Here we show that a common polymorphism in the serotonin transporter gene relates to an accurate and robust neural tracking of speech stimuli in the subcortical auditory pathway. This indicates that serotonin transporter expression, eventually in combination with other polymorphisms, delimits the extent to which lifetime experience shapes the subcortical encoding of speech.
Physiological and Perceptual Sensory Attenuation Have Different Underlying Neurophysiological Correlates
Authors: Palmer Clare E. , Davare Marco , Kilner James M. 
Published: October 2016

Sensory attenuation, the top-down filtering or gating of afferent information, has been extensively studied in two fields: physiological and perceptual. Physiological sensory attenuation is represented as a decrease in the amplitude of the primary and secondary components of the somatosensory evoked potential (SEP) before and during movement. Perceptual sensory attenuation, described using the analogy of a persons' inability to tickle oneself, is a reduction in the perception of the afferent input of a self-produced tactile sensation due to the central cancellation of the reafferent signal by the efference copy of the motor command to produce the action. The fields investigating these two areas have remained isolated, so the relationship between them is unclear. The current study delivered median nerve stimulation to produce SEPs during a force-matching paradigm (used to quantify perceptual sensory attenuation) in healthy human subjects to determine whether SEP gating correlated with the behavior. Our results revealed that these two forms of attenuation have dissociable neurophysiological correlates and are likely functionally distinct, which has important implications for understanding neurological disorders in which one form of sensory attenuation but not the other is impaired. Time–frequency analyses revealed a negative correlation over sensorimotor cortex between gamma-oscillatory activity and the magnitude of perceptual sensory attenuation. This finding is consistent with the hypothesis that gamma-band power is related to prediction error and that this might underlie perceptual sensory attenuation.SIGNIFICANCE STATEMENTWe demonstrate that there are two functionally and mechanistically distinct forms of sensory gating. The literature regarding somatosensory evoked potential (SEP) gating is commonly cited as a potential mechanism underlying perceptual sensory attenuation; however, the formal relationship between physiological and perceptual sensory attenuation has never been tested. Here, we measured SEP gating and perceptual sensory attenuation in a single paradigm and identified their distinct neurophysiological correlates. Perceptual and physiological sensory attenuation has been shown to be impaired in various patient groups, so understanding the differential roles of these phenomena and how they are modulated in a diseased state is very important for aiding our understanding of neurological disorders such as schizophrenia, functional movement disorders, and Parkinson's disease.
Conditional Deletion of the L-Type Calcium Channel Cav1.2 in Oligodendrocyte Progenitor Cells Affects Postnatal Myelination in Mice
Authors: Cheli Veronica T. , Santiago González Diara A. , Namgyal Lama Tenzing , Spreuer Vilma , Handley Vance , Murphy Geoffrey G. , Paez Pablo M. 
Published: October 2016

To determine whether L-type voltage-operated Ca2+channels (L-VOCCs) are required for oligodendrocyte progenitor cell (OPC) development, we generated an inducible conditional knock-out mouse in which the L-VOCC isoform Cav1.2 was postnatally deleted in NG2-positive OPCs. A significant hypomyelination was found in the brains of the Cav1.2 conditional knock-out (Cav1.2KO) mice specifically when the Cav1.2 deletion was induced in OPCs during the first 2 postnatal weeks. A decrease in myelin proteins expression was visible in several brain structures, including the corpus callosum, cortex, and striatum, and the corpus callosum of Cav1.2KOanimals showed an important decrease in the percentage of myelinated axons and a substantial increase in the meang-ratio of myelinated axons. The reduced myelination was accompanied by an important decline in the number of myelinating oligodendrocytes and in the rate of OPC proliferation. Furthermore, using a triple transgenic mouse in which all of the Cav1.2KOOPCs were tracked by aCrereporter, we found that Cav1.2KOOPCs produce less mature oligodendrocytes than control cells. Finally, live-cell imaging in early postnatal brain slices revealed that the migration and proliferation of subventricular zone OPCs is decreased in the Cav1.2KOmice. These results indicate that the L-VOCC isoform Cav1.2 modulates oligodendrocyte development and suggest that Ca2+influx mediated by L-VOCCs in OPCs is necessary for normal myelination.SIGNIFICANCE STATEMENTOverall, it is clear that cells in the oligodendrocyte lineage exhibit remarkable plasticity with regard to the expression of Ca2+channels and that perturbation of Ca2+homeostasis likely plays an important role in the pathogenesis underlying demyelinating diseases. To determine whether voltage-gated Ca2+entry is involved in oligodendrocyte maturation and myelination, we used a conditional knock-out mouse for voltage-operated Ca2+channels in oligodendrocyte progenitor cells. Our results indicate that voltage-operated Ca2+channels can modulate oligodendrocyte development in the postnatal brain and suggest that voltage-gated Ca2+influx in oligodendroglial cells is critical for normal myelination. These findings could lead to novel approaches to intervene in neurodegenerative diseases in which myelin is lost or damaged.
Gi-DREADD Expression in Peripheral Nerves Produces Ligand-Dependent Analgesia, as well as Ligand-Independent Functional Changes in Sensory Neurons
Authors: Saloman Jami L. , Scheff Nicole N. , Snyder Lindsey M. , Ross Sarah E. , Davis Brian M. , Gold Michael S. 
Published: October 2016

Designer receptors exclusively activated by designer drugs (DREADDs) are an advanced experimental tool that could potentially provide a novel approach to pain management. In particular, expression of an inhibitory (Gi-coupled) DREADD in nociceptors might enable ligand-dependent analgesia. To test this possibility, TRPV1-cre mice were used to restrict expression of Gi-DREADDs to predominantly C-fibers. Whereas baseline heat thresholds in both male and female mice expressing Gi-DREADD were normal, 1 mg/kg clozapine-N-oxide (CNO) produced a significant 3 h increase in heat threshold that returned to baseline by 5 h after injection. Consistent with these behavioral results, CNO decreased action potential firing in isolated sensory neurons from Gi-DREADD mice. Unexpectedly, however, the expression of Gi-DREADD in sensory neurons caused significant changes in voltage-gated Ca2+and Na+currents in the absence of CNO, as well as an increase in Na+channel (NaV1.7) expression. Furthermore, CNO-independent excitatory and inhibitory second-messenger signaling was also altered in these mice, which was associated with a decrease in the analgesic effect of endogenous inhibitory G-protein-coupled receptor activation. These results highlight the potential of this exciting technology, but also its limitations, and that it is essential to identify the underlying mechanisms for any observed behavioral phenotypes.SIGNIFICANCE STATEMENTDREADD technology is a powerful tool enabling manipulation of activity and/or transmitter release from targeted cell populations. The purpose of this study was to determine whether inhibitory DREADDs in nociceptive afferents could be used to produce analgesia, and if so, how. DREADD activation produced a ligand-dependent analgesia to heatin vivoand a decrease in neuronal firing at the single-cell level. However, we observed that expression of Gi-DREADD also causes ligand-independent changes in ion channel activity and second-messenger signaling. These findings highlight both the potential and the limitations of this exciting technology as well as the necessity to identify the mechanisms underlying any observed phenotype.
Interactive effects between nest microclimate and nest vegetation structure confirm microclimate thresholds for Lesser Prairie-Chicken nest survival
Authors: Grisham Blake A. , Godar Alixandra J. , Boal Clint W. , Haukos David A. 
Published: October 2016

AbstractThe range of Lesser Prairie-Chickens (Tympanuchus pallidicinctus) spans 4 unique ecoregions along 2 distinct environmental gradients. The Sand Shinnery Oak Prairie ecoregion of the Southern High Plains of New Mexico and Texas is environmentally isolated, warmer, and more arid than the Short-Grass, Sand Sagebrush, and Mixed-Grass Prairie ecoregions in Colorado, Kansas, Oklahoma, and the northeast panhandle of Texas. Weather is known to influence Lesser Prairie-Chicken nest survival in the Sand Shinnery Oak Prairie ecoregion; regional variation may also influence nest microclimate and, ultimately, survival during incubation. To address this question, we placed data loggers adjacent to nests during incubation to quantify temperature and humidity distribution functions in 3 ecoregions. We developed a suite of a priori nest survival models that incorporated derived microclimate parameters and visual obstruction as covariates in Program MARK. We monitored 49 nests in Mixed-Grass, 22 nests in Sand Shinnery Oak, and 30 nests in Short-Grass ecoregions from 2010 to 2014. Our findings indicated that (1) the Sand Shinnery Oak Prairie ecoregion was hotter and drier during incubation than the Mixed- and Short-Grass ecoregions; (2) nest microclimate varied among years within ecoregions; (3) visual obstruction was positively associated with nest survival; but (4) daily nest survival probability decreased by 10% every half-hour when temperature was greater than 34°C and vapor pressure deficit was less than −23 mmHg during the day (about 0600–2100 hours). Our major finding confirmed microclimate thresholds for nest survival under natural conditions across the species' distribution, although Lesser Prairie-Chickens are more likely to experience microclimate conditions that result in nest failures in the Sand Shinnery Oak Prairie ecoregion. The species would benefit from identification of thermal landscapes and management actions that promote cooler, more humid nest microclimates.
Cambio climático y agricultura: una revisión de la literatura con énfasis en América Latina
Authors: López Feldman Alejandro J. , Hernández Cortés Danae 
Published: October 2016

El incremento en la concentración de gases de efecto invernadero es tal que parece inevitable que se presenten cambios en el clima, los cuales forzarán al sector agrícola a tomar medidas de adaptación. Sin embargo, las capacidades de adaptación son limitadas y por lo tanto es muy probable que el cambio climático afecte la disponibilidad y acceso a alimentos e incremente la volatilidad de los precios. En este artículo se presenta una síntesis de la evidencia de los efectos del cambio climático sobre el sector, con énfasis en América Latina. La revisión deja en claro que los efectos serán heterogéneos y que además pueden ser sumamente cuantiosos. Resulta entonces necesario contar con políticas públicas enfocadas en la mitigación de los gases de efecto invernadero, promoviendo al mismo tiempo la adaptación ante el cambio climático. El artículo concluye con algunas consideraciones sobre temaspara investigación futura que puedan contribuir al diseño de dichas políticas públicas.