Assessing the chemical anthropocene - Development of the legacy pollution fingerprint in the North Sea during the last century.

The North Sea and its coastal zones are heavily impacted by anthropogenic activities, which has resulted in significant chemical pollution ever since the beginning of the industrialization in Europe during the 19th century. In order to assess the chemical Anthropocene, natural archives, such as sediment cores, can serve as a valuable data source to reconstruct historical emission trends and to verify the effectiveness of changing environmental legislation. In this study, we investigated 90 contaminants covering inorganic and organic pollutant groups analyzed in a set of sediment cores taken in the North Seas' main sedimentation area (Skagerrak). We thereby develop a chemical pollution fingerprint that records the constant input of pollutants over time and illustrates their continued great relevance for the present. Additionally, samples were radiometrically dated and PAH and PCB levels in porewater were determined using equilibrium passive sampling. Furthermore, we elucidated the origin of lead (Pb) contamination utilizing non-traditional stable isotopic analysis. Our results reveal three main findings: 1. for all organic contaminant groups covered (PAHs, OCPs, PCBs, PBDEs and PFASs) as well as the elements lead (Pb) and titanium (Ti), determined concentrations decreased towards more recent deposited sediment. These decreasing trends could be linked to the time of introductions of restrictions and bans and therefor our results confirm, amongst possible other factors, the effectiveness of environmental legislation by revealing a successive change in contamination levels over the decades. 2. concentration trends for ΣPAH and ΣPCB measured in porewater correspond well with the ones found in sediment which suggests that this method can be a useful expansion to traditional bulk sediment analysis to determine the biologically available pollutant fraction. 3. Arsenic (As) concentrations were higher in younger sediment layers, potentially caused by emissions of corroded warfare material disposed in the study area after WW II.

Maternal absence of the parathyroid hormone 2 receptor affects postnatal pup development.

During the lactation period, mothers have a variety of adaptive changes in brain physiology and behaviour that allow them to properly raise their pups. The exact circuitries and mechanisms responsible for these changes are not fully understood. Recent evidence suggests that the neuropeptide tuberoinfundibular peptide of 39 residues (TIP39) and its receptor, the parathyroid hormone 2 receptor (PTH2-R), contribute to these mechanisms. To further investigate this idea, we evaluated the growth rate of pups from dams with a genetically inactivated PTH2-R (PTH2-R-KO), as well as maternal behavioural and neuroendocrine parameters. We observed that PTH2-R-KO-reared pups had a slowed growth rate. This was associated with a reduced volume of milk yielded by PTH2-R-KO dams after 30-min suckling compared to wild-type (WT) dams when pups were returned after 5 h of separation. Our data suggest a reduced sensitivity of PTH2-R-KO dams to pup stimulation. We also observed a significant reduction in suckling-induced c-Fos expression in the paraventricular hypothalamic nucleus and signs of lower prolactin levels in the PTH2-R-KO dams. Our data suggest that the reduced growth rate of PTH2-R-KO-reared pups was likely the result of alterations in the milk-production pathway rather than modifications in behaviour. Although PTH2-R-KO dams showed increased anxiety in the elevated zero-maze test, no differences from WT dams in maternal behaviour were observed. Taken together, our findings suggest the involvement of the TIP39/PTH2-R system in the pathways involved in the successful development of the pups.

TIP39 modulates effects of novelty-induced arousal on memory.

Tuberoinfundibular peptide of 39 residues (TIP39) is a neuropeptide localized to neural circuits subserving emotional processing. Recent work showed that mice with null mutation for the gene coding TIP39 (TIP39-KO mice) display increased susceptibility to environmental provocation. Based on this stressor-dependent phenotype, the neuroanatomical distribution of TIP39, and knowledge that novelty-induced arousal modulates memory functions via noradrenergic activation, we hypothesized that exposure to a novel environment differently affects memory performance of mice with or without TIP39 signaling, potentially by differences in sensitivity of the noradrenergic system. We tested TIP39-KO mice and mice with null mutation of its receptor, the parathyroid hormone 2 receptor (PTH2-R), in tasks of short-term declarative and social memory (object recognition and social recognition tests, respectively), and of working memory (Y-maze test) under conditions of novelty-induced arousal or acclimation to the test conditions. Mice lacking TIP39 signaling showed memory impairment selectively under conditions of novelty-induced arousal. Acute administration of a PTH2-R antagonist in wild-type mice had a similar effect. The restoration of memory functions in TIP39-KO mice after injection of a ß-adrenoreceptor-blocker, propranolol, suggested involvement of the noradrenergic system. Collectively, these results suggest that the TIP39/PTH2-R system modulates the effects of novelty exposure on memory performance, potentially by acting on noradrenergic signaling.