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Biology subjects

Benz, J.

Publications and source records attributed to Benz, J..

2 recordsLinked to original sources

Grazers and predators mediate the post-settlement bottleneck in Caribbean octocoral forests

Caribbean octocorals have not suffered the decades long decline in abundance that has plagued reef-building scleractinian corals. Their success and the formation of octocoral forests has been attributed to their continuing recruitment to reef habitats. Assessing the processes controlling recruitment is essential to understanding the success of octocorals and predicting their future. Benthic grazers on coral reefs can facilitate the growth and recruitment of corals by reducing the abundance of competitive algal turfs and macroalgae or hinder corals through predation of coral tissue and recruits. We assessed the effects of grazing by fishes and the sea urchin Diadema antillarum and mesofaunal predation on octocoral recruitment in a series of manipulative experiments using varying grazer/predator exclusion and inclusion conditions in in situ and ex situ experiments. Exposure to fish and urchin grazing significantly reduced survival and recruitment of single-polyp octocorals, while turf-associated mesofauna did not significantly affect neither recruitment nor survival. We also found a positive relationship between octocoral recruitment and turf algae, a potential related response to the deleterious effect of grazing exposure. These data suggest that grazers and predators mediate the mortality bottleneck characteristic of recruitment. Thus, the declines in the abundance of grazing fishes and urchins throughout the Caribbean may have contributed to the increase in abundance of octocorals in the Caribbean, concurrent with the loss of scleractinians.

ecology↗

A potent and selective inhibitor for the modulation of MAGL activity in the neurovasculature

Chronic inflammation and blood-brain barrier dysfunction are key pathological hallmarks of neurological disorders such as multiple sclerosis, Alzheimers disease and Parkinsons disease. Major drivers of these pathologies include pro-inflammatory stimuli such as prostaglandins, which are produced in the central nervous system by the oxidation of arachidonic acid in a reaction catalyzed by the cyclooxygenases COX1 and COX2. Monoacylglycerol lipase hydrolyzes the endocannabinoid signaling lipid 2-arachidonyl glycerol, enhancing local pools of arachidonic acid in the brain and leading to cyclooxygenase-mediated prostaglandin production and neuroinflammation. Monoacylglycerol lipase inhibitors were recently shown to act as effective anti-inflammatory modulators, increasing 2-arachidonyl glycerol levels while reducing levels of arachidonic acid and prostaglandins, including PGE2 and PGD2. In this study, we characterized a novel, highly selective, potent and reversible monoacylglycerol lipase inhibitor (MAGLi 432) in a mouse model of lipopolysaccharide-induced blood-brain barrier permeability and in both human and mouse cells of the neurovascular unit: brain microvascular endothelial cells, pericytes and astrocytes. We confirmed the expression of monoacylglycerol lipase in specific neurovascular unit cells in vitro, with pericytes showing the highest expression level and activity. However, MAGLi 432 did not ameliorate lipopolysaccharide-induced blood-brain barrier permeability in vivo or reduce the production of pro-inflammatory cytokines in the brain. Our data confirm monoacylglycerol lipase expression in mouse and human cells of the neurovascular unit and provide the basis for further cell-specific analysis of MAGLi 432 in the context of blood-brain barrier dysfunction caused by inflammatory insults.

neuroscience↗