Dung removal increases under higher dung beetle functional diversity regardless of grazing intensification.

Dung removal by macrofauna such as dung beetles is an important process for nutrient cycling in pasturelands. Intensification of farming practices generally reduces species and functional diversity of terrestrial invertebrates, which may negatively affect ecosystem services. Here, we investigate the effects of cattle-grazing intensification on dung removal by dung beetles in field experiments replicated in 38 pastures around the world. Within each study site, we measured dung removal in pastures managed with low- and high-intensity regimes to assess between-regime differences in dung beetle diversity and dung removal, whilst also considering climate and regional variations. The impacts of intensification were heterogeneous, either diminishing or increasing dung beetle species richness, functional diversity, and dung removal rates. The effects of beetle diversity on dung removal were more variable across sites than within sites. Dung removal increased with species richness across sites, while functional diversity consistently enhanced dung removal within sites, independently of cattle grazing intensity or climate. Our findings indicate that, despite intensified cattle stocking rates, ecosystem services related to decomposition and nutrient cycling can be maintained when a functionally diverse dung beetle community inhabits the human-modified landscape.

Quantifying immediate and delayed effects of anthelmintic exposure on ecosystem functioning supported by a common dung beetle species.

Dung beetles (Coleoptera: Scarabaeoidea) support numerous ecosystem functions in livestock-grazed pastures. Exposure to veterinary anthelmintic residues in livestock dung can have lethal and sublethal effects on dung beetles, and can reduce rates of dung removal, but the immediate and longer-term consequences for other dung beetle mediated functions have rarely been studied. We investigated the consequences of anthelmintic exposure on survival of the dung beetle Aphodius fossor and its delivery of four ecosystems functions that underpin pasture production: dung removal, soil fauna feeding activity, primary productivity, and reduction of soil compaction. We tested whether anthelmintic exposure had immediate or delayed effects on these functions individually and simultaneously (i.e., ecosystem multifunctionality). We found no evidence that ivermectin residues had a lethal effect on adult beetles. For dung removal, we found a significant interaction between the timing of exposure and functioning: while dung removal was impaired by concurrent exposure to high levels of ivermectin, functioning was unaffected when beetles that had been exposed previously to the same concentration of anthelmintic later interacted with untreated dung. Other ecosystem functions were not affected significantly by anthelmintic exposure, and there was no evidence to suggest any persistent impact of anthelmintic exposure on ecosystem multifunctionality. While anthelmintic residues remain a significant threat to dung beetle populations, for adult beetles, we found no evidence that residues have detrimental consequences for ecosystem functioning beyond the immediate point of exposure.

Population structure and history of the Welsh sheep breeds determined by whole genome genotyping.

BACKGROUND: One of the most economically important areas within the Welsh agricultural sector is sheep farming, contributing around £230 million to the UK economy annually. Phenotypic selection over several centuries has generated a number of native sheep breeds, which are presumably adapted to the diverse and challenging landscape of Wales. Little is known about the history, genetic diversity and relationships of these breeds with other European breeds. We genotyped 353 individuals from 18 native Welsh sheep breeds using the Illumina OvineSNP50 array and characterised the genetic structure of these breeds. Our genotyping data were then combined with, and compared to, those from a set of 74 worldwide breeds, previously collected during the International Sheep Genome Consortium HapMap project. RESULTS: Model based clustering of the Welsh and European breeds indicated shared ancestry. This finding was supported by multidimensional scaling analysis (MDS), which revealed separation of the European, African and Asian breeds. As expected, the commercial Texel and Merino breeds appeared to have extensive co-ancestry with most European breeds. Consistently high levels of haplotype sharing were observed between native Welsh and other European breeds. The Welsh breeds did not, however, form a genetically homogeneous group, with pairwise F ST between breeds averaging 0.107 and ranging between 0.020 and 0.201. Four subpopulations were identified within the 18 native breeds, with high homogeneity observed amongst the majority of mountain breeds. Recent effective population sizes estimated from linkage disequilibrium ranged from 88 to 825. CONCLUSIONS: Welsh breeds are highly diverse with low to moderate effective population sizes and form at least four distinct genetic groups. Our data suggest common ancestry between the native Welsh and European breeds. These findings provide the basis for future genome-wide association studies and a first step towards developing genomics assisted breeding strategies in the UK.

Quantitative assessment of microglial morphology and density reveals remarkable consistency in the distribution and morphology of cells within the healthy prefrontal cortex of the rat.

BACKGROUND: Microglial morphology within the healthy brain has been the subject of a number of observational studies. These have suggested that microglia may consist of separate classes, which possess substantially different morphological features. Critically, there have been no systematic quantitative studies of microglial morphology within the healthy brain. METHODS: We examined microglial cells within the adult rat prefrontal cortex. At high magnification, digital reconstructions of cells labelled with the microglial-specific marker ionized calcium-binding adapter molecule-1 (Iba-1) were made in each of the cortical layers. These reconstructions were subsequently analyzed to determine the convex hull area of the cells, their somal perimeter, the length of processes, the number of processes, the extent of process branching and the volume of processes. We additionally examined whether cells' morphological features were associated with cell size or numerical density. RESULTS: Our analysis indicated that while there was substantial variability in the size of cells within the prefrontal cortex, cellular morphology was extremely consistent within each of the cortical layers. CONCLUSIONS: Our results provide quantitative confirmation that microglia are largely homogenous in the uninjured rodent prefrontal cortex.

Chronic stress induces prolonged suppression of the P2X7 receptor within multiple regions of the hippocampus: a cumulative threshold spectra analysis.

A number of studies have identified that mutations in the P2X7 receptor occur with a significantly higher incidence in individuals with major depression. Consistent with these findings, a number of preclinical studies have identified that mice in which the P2X7 receptor has been deleted exhibit a higher level of resilience-like behaviour to acutely aversive situations. At present, however, no studies have examined changes in P2X7 receptor expression in otherwise healthy animals exposed to persistently stressful situations. This is significant as several lines of evidence have demonstrated that it is exposure to persistently aversive, rather than acutely aversive, situations that is associated with the emergence of mood disturbance. Accordingly, the objective of the current study was to examine whether chronic exposure to restraint stress was associated with alterations in the expression of P2X7 within the hippocampal formation. The study involved three principal groups: acute stress (1 session), chronic stress (21 sessions, 1 per day) and a chronic stress with recovery group (21 sessions, 1 per day followed by 7days of no stress) and appropriate control groups. The results of the analysis indicate that all forms of stress, regardless of the duration, provoked a reduction in P2X7 receptor expression. Comparative analysis on normalised data indicated that the magnitude of the P2X7 reduction was significantly greater in the chronic stress relative to the acute stress group. We additionally found that there was a gradual rebound in P2X7 expression, in two of nine regions examined, in animals that were allowed to recover for 7days following the final stress session. Collectively, these findings provide the first evidence that exposure to chronic restraint stress produces a pronounced and relatively persistent suppression of the P2X7 receptor within the hippocampus.

Dynamic structural remodelling of microglia in health and disease: a review of the models, the signals and the mechanisms.

Microglia are unique cells within the central nervous system because of their biophysical independence. As a result of this unusual property the cells must undergo significant structural remodelling in order to engage and connect with other elements within the central nervous system. Efficient remodelling is required for all activities that microglia are involved in ranging from monitoring synaptic information flow through to phagocytosis of tissue debris. Despite the fact that morphological remodelling is a pre-requisite to all microglial activities, relatively little research has been undertaken on the topic. This review examines what is known about how microglia transform themselves during development, under physiological conditions in response to changes in neuronal activity, and under pathological circumstances. Specific attention is given to exploring a variety of models that have been proposed to account for microglial transformation as well as the signals that are known to trigger these transformations.

Neuroinflammation and neuronal loss precede Aß plaque deposition in the hAPP-J20 mouse model of Alzheimer's disease.

Recent human trials of treatments for Alzheimer's disease (AD) have been largely unsuccessful, raising the idea that treatment may need to be started earlier in the disease, well before cognitive symptoms appear. An early marker of AD pathology is therefore needed and it is debated as to whether amyloid-ßAß? plaque load may serve this purpose. We investigated this in the hAPP-J20 AD mouse model by studying disease pathology at 6, 12, 24 and 36 weeks. Using robust stereological methods, we found there is no neuron loss in the hippocampal CA3 region at any age. However loss of neurons from the hippocampal CA1 region begins as early as 12 weeks of age. The extent of neuron loss increases with age, correlating with the number of activated microglia. Gliosis was also present, but plateaued during aging. Increased hyperactivity and spatial memory deficits occurred at 16 and 24 weeks. Meanwhile, the appearance of plaques and oligomeric Aß were essentially the last pathological changes, with significant changes only observed at 36 weeks of age. This is surprising given that the hAPP-J20 AD mouse model is engineered to over-expresses Aß. Our data raises the possibility that plaque load may not be the best marker for early AD and suggests that activated microglia could be a valuable marker to track disease progression.

Chronic stress-induced disruption of the astrocyte network is driven by structural atrophy and not loss of astrocytes.

Chronic stress is well recognized to decrease the number of GFAP⁺ astrocytes within the prefrontal cortex (PFC). Recent research, however, has suggested that our understanding of how stress alters astrocytes may be incomplete. Specifically, chronic stress has been shown to induce a unique form of microglial remodelling, but it is not yet clear whether astrocytes also undergo similar structural modifications. Such alterations may be significant given the role of astrocytes in modulating synaptic function. Accordingly, in the current study we have examined changes in astrocyte morphology following exposure to chronic stress in adult rats, using three-dimensional digital reconstructions of astrocytes. Our analysis indicated that chronic stress produced profound atrophy of astrocyte process length, branching and volume. We additionally examined changes in astrocyte-specific S100ß, which are both a putative astrocyte marker and a protein whose expression is associated with astrocyte distress. While we found that S100ß levels were increased by stress, this increase was not correlated with atrophy. We further established that while chronic stress was associated with a decrease in astrocyte numbers when GFAP labelling was used as a marker, we could find no evidence of a decrease in the total number of cells, based on Nissl staining, or in the number of S100ß⁺ cells. This finding suggests that chronic stress may not actually reduce astrocyte numbers and may instead selectively decrease GFAP expression. The results of the current study are significant as they indicate stress-induced astrocyte-mediated disturbances may not be due to a loss of cells but rather due to significant remodeling of the astrocyte network.

Chronic stress induced remodeling of the prefrontal cortex: structural re-organization of microglia and the inhibitory effect of minocycline.

Recently, it has been discovered that the working memory deficits induced by exposure to chronic stress can be prevented by treating stressed animals with minocycline, a putative inhibitor of microglial activity. One of the pressing issues that now requires clarification is exactly how exposure to chronic stress modifies microglial morphology, this being a significant issue as microglial morphology is tightly coupled with their function. To examine how chronic stress alters microglial morphology, we digitally reconstructed microglia within the rat medial prefrontal cortex. Our analysis revealed that stress increased the internal complexity of microglia, enhancing ramification (i.e. branching) without altering the overall area occupied by the cell and that this effect was more pronounced in larger cells. We subsequently determined that minocycline treatment largely abolished the pro-ramifying effects of stress. With respect to mechanisms, we could not find any evidence of increased inflammation or neurodegeneration (interleukin-1ß, MHC-II, CD68, terminal deoxynucleotidyl transferase dUTP nick end labeling, and activated caspase-3). We did, however, find that chronic stress markedly increased the expression of ß1-integrin (CD29), a protein previously implicated in microglial ramification. Together, these findings highlight that increased ramification of microglia may represent an important neurobiological mechanism through which microglia mediate the behavioral effects of chronic psychological stress.

Correlations of the Gait Profile Score and the Movement Analysis Profile relative to clinical judgments.

The Gait Profile Score (GPS) is a single index measure that summarises the overall deviation of kinematic gait data relative to normative data. The GPS can be decomposed to provide Gait Variable Scores (GVS) of nine key component kinematic gait variables, which are presented as a Movement Analysis Profile (MAP). The purpose of this study was to investigate the validity of the GPS and MAP relative to clinician judgments. Kinematic data were selected from 60 children and inspected by 17 experienced clinicians. The degree of abnormality of the overall unilateral gait pattern and the nine kinematic variables was rated according to a 0-10 point scale. Strong, significant, positive correlations were found between the GPS and MAP component scores, and clinicians' ratings of kinematic gait deviation, with Spearman correlations ranging from 0.84 to 0.97. These high correlations provide evidence that the GPS and the MAP have criterion-related validity relative to clinician judgments. We propose that the GPS and particularly its MAP decomposition may be useful in clinical practice and education as an adjunct to the traditional presentation of complex kinematic data.

The gait profile score and movement analysis profile.

The Gait Deviation Index (GDI) has been proposed as an index of overall gait pathology. This study proposes an interpretation of the difference measure upon which the GDI is based, which naturally leads to the definition of a similar index, the Gait Profile Score (GPS). The GPS can be calculated independently of the feature analysis upon which the GDI is based. Understanding what the underlying difference measure represents also suggests that reporting a raw score, as the GPS does, may have advantages over the logarithmic transformation and z-scaling incorporated in the GDI. It also leads to the concept of a Movement Analysis Profile (MAP) to summarise much of the information contained within kinematic data. A validation study on all children attending a paediatric gait analysis service over 3 years (407 children) provides evidence to support the use of the GPS through analysis of its frequency distribution across different Gross Motor Function Classification System (GMFCS) and Gillette Functional Assessment Questionnaire (FAQ) categories, investigation of intra-session variability, and correlation with the square root of GGI. Correlation with GDI confirms the strong relationship between the two measures. The study concludes that GDI and GPS are alternative and closely related measures. The GDI has prior art and is particularly useful in applications arising out of feature analysis such as cluster analysis or subject matching. The GPS will be easier to calculate for new models where a large reference dataset is not available and in association with applications using the MAP.