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Ecological communities used in biological pest control are usually represented as three-trophic level food chains with top-down control. However, at least two factors complicate this simple way of characterizing agricultural communities. First, agro-ecosystems are composed of several interacting species forming complicated food webs. Second, the structure of agricultural communities may vary in time. Efficient pest management approaches need to integrate these two factors to generate better predictions for pest control. In this work, we identified the food web components of an avocado agro-ecosystem, and unravelled patterns of co-occurrence and interactions between these components through field and laboratory experiments. This allowed us to predict community changes that would improve the performance of the naturally occurring predators and to test these predictions in field population experiments. Field surveys revealed that the food-web structure and species composition of the avocado community changed in time. In spring, the community was characterized by a linear food chain of Euseius stipulatus, an omnivorous mite, feeding on pollen. In the summer, E. stipulatus and a predatory mite, Neoseiulus californicus, shared a herbivorous mite prey. Laboratory experiments confirmed these trophic interactions and revealed that N. californicus can feed inside the prey nests, whereas E. stipulatus cannot, which may further reduce competition among predators. Finally, we artificially increased the coexistence of the two communities via addition of the non-herbivore food source (pollen) for the omnivore. This led to an increase in predator numbers and reduced populations of the herbivore. Therefore, the presence of pollen is expected to improve pest control in this system. [ABSTRACT FROM AUTHOR]

We evaluated the influence of six different citrus rootstocks on the incidence of the citrus leafminer, Phyllocnistis citrella Stainton (Lepidoptera: Gracillariidae), and the aphid species, Aphisgossypii Glover and A. spiraecola Patch (Hemiptera: Aphididae), on 'Clementine de Nules' trees (Citrus clementina Hort. ex Tan.). Sampling was conducted during 2005 and 2006 in a grove of 3-yr-old trees in southern Spain with six rootstocks arranged in a completely randomized block design. Incidence (i.e., degree of infestation) and availability of resources for herbivores were assessed bi-weekly, and in addition, a "flushing index" was estimated as the number of young shoots (as a percentage of total shoots) susceptible to herbivore injury. Our results showed that contrasting factors affected the incidence of populations of P. citrella, A. gossypii, and A. spiraecola on 'Clementine de Nules'. Incidence of P. citrella was significantly dependent on the flushing pattern observed throughout the study, whereas the reverse was true for the aphid species. Among these, A. spiraecola had similar levels of incidence regardless of rootstock, whereas A. gossypii were found almost exclusively on leaves of 'Clementine de Nules' grafted on 'Cleopatra mandarin' (Citrus reshni Hort. ex Tan). Potential implications of these results on pest control are discussed. [ABSTRACT FROM AUTHOR]

We have studied a group of twenty-seven patients who suffer allergic reactions to vespids stings. Specific IgE antibodies to venom extracts from Polistes gallicus and Vespula germanica were measured by RAST, and the crossreactivity between the two venoms was compared using the RAST inhibition technique. We concluded that, in southern Spain, sensitization to P. gallicus was more prevalent than that to V. germanica, with 44% of the subjects in this study reacting to P. gallicus compared with 33% to V. germanica. However, there was a considerable degree of crossreactivity between the two species. It is evident that Polistes is an important species in this area; however, both in Spain and other Mediterranean countries, V. germanica venom is used almost exclusively for diagnosis and immunotherapy. [ABSTRACT FROM AUTHOR]

Background and Purpose: The sigma-1 (σ(1) ) receptor is a ligand-regulated molecular chaperone that has been involved in pain, but there is limited understanding of the actions associated with its pharmacological modulation. Indeed, the selectivity and pharmacological properties of σ(1) receptor ligands used as pharmacological tools are unclear and the demonstration that σ(1) receptor antagonists have efficacy in reversing central sensitization-related pain sensitivity is still missing., Experimental Approach: The pharmacological properties of a novel σ(1) receptor antagonist (S1RA) were first characterized. S1RA was then used to investigate the effect of pharmacological antagonism of σ(1) receptors on in vivo nociception in sensitizing conditions and on in vitro spinal cord sensitization in mice. Drug levels and autoradiographic, ex vivo binding for σ(1) receptor occupancy were measured to substantiate behavioural data., Key Results: Formalin-induced nociception (both phases), capsaicin-induced mechanical hypersensitivity and sciatic nerve injury-induced mechanical and thermal hypersensitivity were dose-dependently inhibited by systemic administration of S1RA. Occupancy of σ(1) receptors in the CNS was significantly correlated with the antinociceptive effects. No pharmacodynamic tolerance to the antiallodynic and antihyperalgesic effect developed following repeated administration of S1RA to nerve-injured mice. As a mechanistic correlate, electrophysiological recordings demonstrated that pharmacological antagonism of σ(1) receptors attenuated the wind-up responses in spinal cords sensitized by repetitive nociceptive stimulation., Conclusions and Implications: These findings contribute to evidence identifying the σ(1) receptor as a modulator of activity-induced spinal sensitization and pain hypersensitivity, and suggest σ(1) receptor antagonists as potential novel treatments for neuropathic pain., (© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.)

Theiler's murine encephalomyelitis virus (TMEV) disease is induced following intracerebral inoculation of TMEV, a member of picornavirus family, in susceptible animals. The pathogenesis of paralytic syndrome is associated with a chronic progressive demyelinating disease characterized by perivascular of immune inflammatory cells. Although TMEV induced demyelinating disease (TMEV IDD) is initiated by virus specific CD4+ T cells targeting CNS persistent virus, CD4+ T cell responses against self myelin epitopes activated via epitope spreading contribute to chronic disease pathogenesis. In the present report we delineated possible pathogenic mechanisms related with inflammatory process, leading to demyelination and axonal loss. The importance of proinflammatory cytokines in sustaining the inflammatory process and cause direct oligodendrotoxicity is emphasized. Different approaches in therapeutic strategies affecting cytokines are also presented.

Maturation of oligodendrocyte progenitors (O2A) is characterized by morphological changes and the sequential expression of specific antigens leading to the formation of myelin membrane. Monoclonal antibodies A2B5, A007, anti-vimentin, and anti-galactocerebroside, recognize oligodendroglia at different stages of development. The neuroepithelial precursor marker nestin is also expressed by the oligodendroglial lineage; we have used enriched populations of progenitors isolated from neonatal rat brain cultures to further examine the cellular distribution of this intermediate filament protein. The phenotypic distribution of nestin positive cells among the oligodendrocyte lineage showed that 65% reacted with A2B5, whereas only 5% were A007(+), and 4% galactocerebroside(+). The remaining 25% of the cells were not labeled and had small cellular bodies devoid of processes, characteristic of the pre-O2A progenitor. Further analysis of the nestin(+) population showed that the majority of the cells were also vimentin(+). Antibody-dependent complement mediated cytolysis of A2B5(+) (O2A cells) and galactocerebroside(+) (mature oligodendrocytes) cells left a population of nestin(+) cells that were induced to proliferate in the presence of growth factors and to differentiate into A2B5(+) and galactocerebroside(+) cells. Proliferating cells maintained in the presence of platelet-derived growth factor or basic fibroblast growth factor retained nestin expression along with A2B5. By contrast, in serum-free medium nestin expression decreased while postmitotic cells acquired A007 and galactocerebroside. Our results suggest that nestin expression is a marker of pre-O2A cells that is maintained in proliferating glial progenitors, but is quickly down-regulated in postmitotic oligodendrocytes (A007(+)/galacto-cerebroside(+)) along with A2B5 and vimentin. However, other glial cells including type 2 astrocytes and some amoeboid microglia also share nestin expression., (Copyright 2001 Wiley-Liss, Inc.)

Proinflammatory mediators have been implicated in demyelinating disorders, including multiple sclerosis, whereas it has been proposed that the anti-inflammatory cytokines interleukin- (IL-) 4 and IL-10 participate in disease recovery. The present study analysed the effect of interferon-gamma (IFN-gamma) and bacterial endotoxin (lipopolysaccharide, LPS) on proliferation and survival of progenitors and differentiated oligodendrocytes. We also investigated the presence of receptors for IL-4 and IL-10 in oligodendroglial cells and explored a possible protective action of IL-4 and IL-10 in cultures following LPS/IFN-gamma. Finally, the role of endogenous nitric oxide (NO) on cell viability and the modulatory action of IL-4 and IL-10 on inducible nitric oxide synthase (iNOS) expression were also analysed. We report that LPS and/or IFN-gamma reduced proliferation and viability of oligodendroglial cells. Cell death, presumably by apoptosis as evidence by TUNEL and Annexin V binding, was observed following LPS/IFN-gamma, progenitors being more sensitive than differentiated cells. At both developmental stages, LPS/IFN-gamma-treated cultures expressed iNOS protein and released micromolar concentrations of NO. In progenitors, LPS/IFN-gamma-mediated cell damage was partially dependent on endogenous NO production, whereas NO was fundamental for cytotoxicity of differentiated oligodendrocytes. Both cell types expressed mRNA for IL-4 and IL-10 receptors and expression of IL-10 receptors at the protein level was also demonstrated. Treatment with either cytokine inhibited the expression of iNOS resulting from the proinflammatory stimulation. IL-10 was more effective than IL-4 in suppressing iNOS expression and, interestingly, IL-10 conferred protection against oligodendroglial death evoked by LPS/IFN-gamma. Our data raise the question of whether IL-10 may play a protective role in demyelinating diseases, not only downregulating the function of inflammatory cells but also promoting survival of progenitors and differentiated oligodendrocytes.

The nucleoside triphosphatase (NTPase), nucleoside diphosphatase (NDPase), 5'-nucleotidase (5'-Nase), and purine nucleoside phosphorylase (PNPase) activity has been examined in the cerebral cortex, subcortical white matter, and hippocampus from embryonic day (E)16 to postnatal day (P)18. Microglia display all four purine-related enzymatic activities, but the expression of these enzymatic activities differed depending on the distinct microglial typologies observed during brain development. We have identified three main morphologic typologies during the process of microglial differentiation: ameboid microglia (parenchymatic precursors), primitive ramified microglia (intermediate forms), and resting microglia (differentiated cells). Ameboid microglia, which were encountered from E16 to P12, displayed the four enzymatic activities. However, some ameboid microglial cells lacked 5'-Nase activity in gray matter, and some were PNPase-negative in both gray and white matter. Primitive ramified microglia were already observed in the embryonic period but mostly distributed during the first 2 postnatal weeks. These cells expressed NTPase, NDPase, 5'-Nase, and PNPase. Similar to ameboid microglia, we found primitive ramified microglia lacking the 5'-Nase and PNPase activities. Resting microglia, which were mostly distinguishable from the third postnatal week, expressed NTPase and NDPase, but they lacked or displayed very low levels of 5'-Nase activity, and only a subpopulation of resting microglia was PNPase-positive. Apart from cells of the microglial lineage, GFAP-positive astrocytes and radial glia cells were also labeled by the PNPase histochemistry. As shown by our results, the differentiation process from cell precursors into mature microglia is accompanied by changes in the expression of purine-related enzymes. We suggest that the enzymatic profile and levels of the different purine-related enzymes may depend not only on the differentiation stage but also on the nature of the cells. The use of purine-related histoenzymatic techniques as a microglial markers and the possible involvement of microglia in the control of extracellular purine levels during development are also discussed.

Jimpy is a shortened life-span murine mutant showing recessive sex-linked inheritance. The genetic defect consists of a point mutation in the PLP gene and produces a severe CNS myelin deficiency that is associated with a variety of complex abnormalities affecting all glial populations. The myelin deficiency is primarily due to a failure to produce the normal amount of myelin during development. However, myelin destruction and oligodendrocyte death also account for the drastic myelin deficit observed in jimpy. The oligodendroglial cell line shows complex abnormalities in its differentiation pattern, including the degeneration of oligodendrocytes through an apoptotic mechanism. Oligodendrocytes seem to be the most likely candidate to be primarily altered in a disorder affecting myelination, but disturbances affecting astrocytes and microglia are also remarkable and may have a crucial significance in the development of the jimpy disorder. In fact, the jimpy phenotype may not be attributed to a defect in a single cell but rather to a deficiency in the normal relations between glial cells. Evidences from a variety of sources indicate that the jimpy mutant could be a model for disturbed glial development in the CNS. The accurate knowledge of the significance of PLP and its regulation during development must be of vital importance in order to understand glial abnormalities in jimpy.

Several studies agree that microglial cells derive from monocytes that infiltrate the central nervous system during development, but the precise mechanism by which these cells enter into the nervous tissue is still unknown. In this way, the aim of the present study was to analyze the expression of two cell adhesion molecules involved in the recruitment of blood leukocytes into tissues, the lymphocyte function-associated antigen-1alpha (LFA-1alpha) and the intercellular adhesion molecule-1 (ICAM-1) in the developing rat brain (from E16 to P18). By means of immunohistochemistry, our observations showed that LFA-1alpha and ICAM-1 were expressed in the developing rat brain with a definite distribution pattern and a characteristic time course of appearance. In the embryonic period, LFA-1alpha immunoreactivity was displayed not only by intravascular blood cells but also by intraparenchymal round cells with a horseshoe-shaped nucleus, showing the typical morphological features of monocytes. Monocyte-like cells present in the embryonic brain parenchyma often displayed mitotic profiles. LFA-1alpha immunohistochemistry also revealed the presence of some LFA-1alpha-positive cells belonging to the ameboid microglial population (mostly in the white matter from E18). In the postnatal period, LFA-1alpha immunoreactivity was displayed by some ameboid microglial cells (P0-P9) and also by some ramified microglia. LFA-1alpha immunoreactivity observed in ramified microglia was weaker when compared to LFA-1alpha stained ameboid microglia. In contrast, ICAM-1 immunolabeling during the embryonic period was mainly located in endothelial cells of parenchymal brain blood vessels (principally from day E18). Blood vessels in choroid plexus and meninges also expressed ICAM-1 during the embryonic time. In postnatal animals, ICAM-1 immunoreactivity was found in relation to endothelial cells of blood vessels, but the density of ICAM-1-positive blood vessels was lower than that during the embryonic period. The gradual regulation in the expression of LFA-1alpha by monocyte-like cells and cells of the microglial lineage, and the expression of ICAM-1 by the brain vasculature strongly suggest that the LFA-1/ICAM-1 system may be a mechanism involved in the entry of microglial cell precursors into the developing rat brain.

The morphology and distribution of microglial cells were studied in the normal cerebellum of young and adult mice using the histochemical demonstration of nucleoside diphosphatase as a specific microglial marker. Our results showed that microglial cells were present in all cerebellular lobules of both young and adult mice, but their distribution and morphology were not homogeneous throughout the cerebellum. Heterogeneity in microglial cell distribution was exclusively related to their location in the different histological layers, and no significant differences were found either between the different cerebellar lobules or between young and adult mice. Microglial density was higher in the cerebellar nuclei than in the cortex; within the cortex, the molecular layer was less densely populated by microglial cells than the granular layer and the white matter. The morphological study revealed that microglial cells were ramified in all cerebellar lobules of both young and adult mice but showed different sizes and ramification patterns as a function of their specific location in the different histological layers. Several typologies of microglial cells were described on the basis of observations in both horizontal and coronal sections. The specific layer-related pattern of microglial distribution and morphology in mouse cerebellum strongly suggests a physical and functional adaptation of these cells to the characteristics of their microenvironment.

The histochemical demonstration of nucleoside diphosphatase as a specific microglial marker was used to study the distribution of this glial cell type in the cerebral cortex of Podarcis muralis and Podarcis hispanica. Our results showed that in both species, NDPase staining was specific for the microglial cell population and that microglial cells displayed a specific localization pattern in the different cortical areas. In the medal cortex, microglial cells were principally found in the outer and inner plexiform layers in the strata adjacent to the granular layer. Moreover, some microglial cells were found near the ependymal layer, but no microglial cells were normally present near the brain surface and never in the deep inner plexiform layer. In the dorsomedial cortex, microglial cells were found near the brain surface in the outer plexiform layer, in the upper part of the granular layer, and near the ependymal layer. No microglial cells were found, however, in the outer and inner plexiform layers adjacent to the granular layer. Finally, in the dorsolateral cortex, microglial cells were located in the upper part of the outer plexiform layer, in and bordering the granular layer, and scattered in the inner plexiform layer. This layered-pattern distribution of microglial cell population in the cerebral cortex of the lizard differs from the apparently homogeneous distribution of microglia in the brain of mammals.