836 research outputs found
Bypassing use-dependent plasticity in the primary motor cortex to preserve adaptive behavior.
Behavioral adaptation, a central feature of voluntary movement, is known to rely on top-down cognitive control. For example, the conflict-adaptation effect on tasks such as the Stroop task leads to better performance (e.g. shorter reaction time) for incongruent trials following an already incongruent one. The role of higher-order cortices in such between-trial adjustments is well documented, however, a specific involvement of the primary motor cortex (M1) has seldom been questioned. Here we studied changes in corticospinal excitability associated with the conflict-adaptation process. For this, we used single-pulse transcranial-magnetic stimulation (TMS) applied between two consecutive trials in an interference flanker task, while measuring motor-evoked potentials (MEPs) after agonistic and antagonistic voluntary movements. In agonist movement, MEP amplitude was modulated by recent movement history with an increase favoring movement repetition, but no significant change in MEP size was observed whether a previous trial was incongruent or congruent. Critically, for an antagonist movement, the relative size of MEPs following incongruent trials correlated positively with the strength of behavioral adaptation measured as the degree of RT shortening across subjects. This post-conflict increase in corticospinal excitability related to antagonist muscle recruitment could compensate for a potential deleterious bias due to recent movement history that favors the last executed action. Namely, it prepares the motor system to rapidly adapt to a changing and unpredictable context by equalizing the preparation for all possible motor responses
Consequences of an ecosystem state shift for nitrogen cycling in a desert stream
Cessation of cattle grazing has resulted in the reestablishment of wetlands in some streams of the U.S. Southwest. Decades of cattle grazing prevented vascular plant growth in Sycamore Creek (Arizona, U.S.A.), resulting in stream reaches dominated by diatoms and filamentous green algae. Establishment of vascular plants can profoundly modify ecosystem processes; yet, the effects on nitrogen (N) cycling remain unexplored. We examined the consequences of this ecosystem state shift on N cycling in this N-limited desert stream. We compared results from whole-reach ammonium-N stable isotope (15NH4+) tracer additions conducted before (pre-wetland state) and 13 yr after (wetland state) free-range cattle removal from the watershed. Water column estimations showed that in-stream N uptake and storage were higher in the pre-wetland than in the wetland state. N turnover was also higher in the pre-wetland state, indicating that assimilated N was retained for shorter time in stream biomass. In addition, N uptake was mostly driven by assimilatory uptake regardless of the ecosystem state considered. Water column trends were mechanistically explained by the fact that the dominant primary uptake compartments in the pre-wetland state (i.e., algae and diatoms) had higher assimilatory uptake and turnover rates than those in the wetland state (i.e., vascular plants). Overall, results show that the shift in the composition and dominance of primary producers induced by the cessation of cattle grazing within the stream-riparian corridor changes in-stream N processing from a dominance of intense and fast N recycling to a prevalence of N retention in biomass of primary producers
In Vitro Intracellular Trafficking of Virulence Antigen during Infection by Yersinia pestis
Yersinia pestis, the causative agent of plague, encodes several essential virulence factors on a 70 kb plasmid, including the Yersinia outer proteins (Yops) and a multifunctional virulence antigen (V). V is uniquely able to inhibit the host immune response; aid in the expression, secretion, and injection of the cytotoxic Yops via a type III secretion system (T3SS)-dependent mechanism; be secreted extracellularly; and enter the host cell by a T3SS-independent mechanism, where its activity is unknown. To elucidate the intracellular trafficking and target(s) of V, time-course experiments were performed with macrophages (MΦs) infected with Y. pestis or Y. pseudotuberculosis at intervals from 5 min to 6 h. The trafficking pattern was discerned from results of parallel microscopy, immunoblotting, and flow cytometry experiments. The MΦs were incubated with fluorescent or gold conjugated primary or secondary anti-V (antibodies [Abs]) in conjunction with organelle-associated Abs or dyes. The samples were observed for co-localization by immuno-fluorescence and electron microscopy. For fractionation studies, uninfected and infected MΦs were lysed and subjected to density gradient centrifugation coupled with immunoblotting with Abs to V or to organelles. Samples were also analyzed by flow cytometry after lysis and dual-staining with anti-V and anti-organelle Abs. Our findings indicate a co-localization of V with (1) endosomal proteins between 10–45 min of infection, (2) lysosomal protein(s) between 1–2 h of infection, (3) mitochondrial proteins between 2.5–3 h infection, and (4) Golgi protein(s) between 4–6 h of infection. Further studies are being performed to determine the specific intracellular interactions and role in pathogenesis of intracellularly localized V
Note sur un élevage d'oies des Landes avec essais de production des foies gras à Madagascar
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Learned vocal variation is associated with abrupt cryptic genetic change in a parrot species complex
<div><p>Contact zones between subspecies or closely related species offer valuable insights into speciation processes. A typical feature of such zones is the presence of clinal variation in multiple traits. The nature of these traits and the concordance among clines are expected to influence whether and how quickly speciation will proceed. Learned signals, such as vocalizations in species having vocal learning (e.g. humans, many birds, bats and cetaceans), can exhibit rapid change and may accelerate reproductive isolation between populations. Therefore, particularly strong concordance among clines in learned signals and population genetic structure may be expected, even among continuous populations in the early stages of speciation. However, empirical evidence for this pattern is often limited because differences in vocalisations between populations are driven by habitat differences or have evolved in allopatry. We tested for this pattern in a unique system where we may be able to separate effects of habitat and evolutionary history. We studied geographic variation in the vocalizations of the crimson rosella (<em>Platycercus elegans</em>) parrot species complex. Parrots are well known for their life-long vocal learning and cognitive abilities. We analysed contact calls across a <em>ca</em> 1300 km transect encompassing populations that differed in neutral genetic markers and plumage colour. We found steep clinal changes in two acoustic variables (fundamental frequency and peak frequency position). The positions of the two clines in vocal traits were concordant with a steep cline in microsatellite-based genetic variation, but were discordant with the steep clines in mtDNA, plumage and habitat. Our study provides new evidence that vocal variation, in a species with vocal learning, can coincide with areas of restricted gene flow across geographically continuous populations. Our results suggest that traits that evolve culturally can be strongly associated with reduced gene flow between populations, and therefore may promote speciation, even in the absence of other barriers.</p> </div
Transformation, adaptation and development: relating concepts to practice
In recent years there has been a growing number of academic reviews discussing the theme of transformation and its association with adaptation to climate change. On the one hand this has stimulated exchange of ideas and perspectives on the parameters of transformation, but it has also given rise to confusion in terms of identifying what constitutes a non-incremental form of adaptation on the ground. What this article aims to do instead is help researchers and practitioners relate different interpretations of transformation to practice by proposing a typological framework for categorising forms of change that focuses on mechanisms and objectives. It then discusses how these categorisations link to the broader conceptions and critiques noted above, with the idea that this will enable those who seek to analyse or plan adaptation to better analyse what types of action are potentially constitutive of transformation. In doing so, it should equally assist in the identification and specification of critical questions that need to be asked of such activity in relation to issues of sustainability and equity. As the term transformation gains ground in discussions of climate change adaptation, it is necessary to take a step back, review quite what commentators mean when they use the word, and consider the implications on people, especially the most vulnerable and marginalised, of “doing” or promoting transformation in its different forms
TCR signal strength controls thymic differentiation of discrete proinflammatory gamma delta T cell subsets
The mouse thymus produces discrete gd T cell subsets that make either interferon-g (IFN-g) or interleukin 17 (IL-17), but the role of the T cell antigen receptor (TCR) in this developmental process remains controversial. Here we show that Cd3g+/− Cd3d+/− (CD3 double-haploinsufficient (CD3DH)) mice have reduced TCR expression and signaling strength on gd T cells. CD3DH mice had normal numbers and phenotypes of ab thymocyte subsets, but impaired differentiation of fetal Vg6+ (but not Vg4+) IL-17- producing gd T cells and a marked depletion of IFN-g-producing CD122+ NK1.1+ gd T cells throughout ontogeny. Adult CD3DH mice showed reduced peripheral IFN-g+ gd T cells and were resistant to experimental cerebral malaria. Thus, TCR signal strength within specific thymic developmental windows is a major determinant of the generation of proinflammatory gd T cell subsets and their impact on pathophysiology
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