摘要: Anthropogenic noise can affect a number of behavioral, physiological, and ecological aspects of animals from major taxonomic groups, raising serious conservation concerns. For example, noise pollution impacts communicative behavior and perception of signals, movements and distribution, as well as predator-prey interactions, such as hunting success or predator detection and predation risk assessment. We have carried out an experimental playback study, in which we investigated whether exposure to anthropogenic noise (sound of a tractor) distracts free-ranging barn swallows Hirundo rustica from paying attention to an approaching human predator (the cognitive distraction hypothesis), or whether noise leads to increased responsiveness to this predator (the increased threat hypothesis). The subjects were male barn swallows attending their breeding territories during the time when the females were incubating. We found that barn swallow males initiated flight at significantly greater distances to the approaching human predator in the noise treatment than during the quiet control trials. These results suggest that anthropogenic noise causes increased vigilance and reactivity rather than a distraction, enabling birds to avoid the predator more quickly. We further discuss the mechanism behind the increased alertness in response to noise and contrast the increased threat mechanism, usually tested in previous studies, with an alternative cognitive sensitization mechanism.

摘要: Microglia are the primary source of transglutaminase 2 (TGM2) in the brain; however, the roles of microglial TGM2 in neural development and disease are still not well known. The aim of this study is to elucidate the role and mechanisms of microglial TGM2 in the brain. A mouse line with a specific knockout of Tgm2 in microglia was generated. Immunohistochemistry, Western blot and qRT-PCR assays were performed to evaluate the expression levels of TGM2, PSD-95 and CD68. Confocal imaging, immunofluorescence staining and behavioural analyses were conducted to identify phenotypes of microglial TGM2 deficiency. Finally, RNA sequencing, qRT-PCR and co-culture of neurons and microglia were used to explore the potential mechanisms. Deletion of microglial Tgm2 causes impaired synaptic pruning, reduced anxiety and increased cognitive deficits in mice. At the molecular level, the phagocytic genes, such as Cq1a, C1qb and Tim4, are significantly down-regulated in TGM2-deficient microglia. This study elucidates a novel role of microglial TGM2 in regulating synaptic remodelling and cognitive function, indicating that microglia Tgm2 is essential for proper neural development.