Freshwater Seepage Into Sediments of the Shelf, Shelf Edge, and Continental Slope of the Canadian Beaufort Sea

Long‐term warming of the continental shelf of the Canadian Beaufort Sea caused by the transgression associated with the last deglaciation may be causing decomposition of relict offshore subsea permafrost and gas hydrates. To evaluate this possibility, pore waters from 118 sediment cores up to 7.3‐m long were taken on the shelf and slope and analyzed for chloride concentrations and δ180 and δD composition. We observed downcore decreases in pore waters Cl− concentration in sediments from all sites from the inner shelf (<20‐m water depth), from the shelf edge, from the outer slope (down to 1,000‐m water depths), and from localized shelf features such as midshelf pingo‐like features and inner shelf pockmarks. In contrast, pore water freshening is absent from all investigated cores of the Mackenzie Trough. Downcore pore waters Cl− concentration decreases indicate regional widespread freshwater seepage. Extrapolations to zero Cl− of pore water Cl− versus δ180 regression lines indicate that freshwaters in these environments carry different isotope signatures and thus are sourced from different reservoirs. These isotopic signatures indicate that freshening of shelf sediments pore waters is a result of downward infiltration of Mackenzie River water, freshening of shelf edge sediments is due to relict submarine permafrost degradation or gas hydrate decomposition under the shelf, and freshening of slope sediments is consistent with regional groundwater flow and submarine groundwater discharge as far as 150 km from shore. These results confirm ongoing decomposition of offshore permafrost and suggest extensive current groundwater discharge far from the coast

Control of neuronal migration through rostral migratory stream in mice

During the nervous system development, immature neuroblasts have a strong potential to migrate toward their destination. In the adult brain, new neurons are continuously generated in the neurogenic niche located near the ventricle, and the newly generated cells actively migrate toward their destination, olfactory bulb, via highly specialized migratory route called rostral migratory stream (RMS). Neuroblasts in the RMS form chains by their homophilic interactions, and the neuroblasts in chains continually migrate through the tunnels formed by meshwork of astrocytes, glial tube. This review focuses on the development and structure of RMS and the regulation of neuroblast migration in the RMS. Better understanding of RMS migration may be crucial for improving functional replacement therapy by supplying endogenous neuronal cells to the injury sites more efficiently

Leukemia inhibitory factor inhibits neuronal terminal differentiation through STAT3 activation

The discovery of stem cells in the adult central nervous system raises questions concerning the neurotrophic factors that regulate postnatal neuronal development. Olfactory receptor neurons (ORNs) are a useful model, because they are capable of robust neurogenesis throughout adulthood. We have investigated the role of leukemia inhibitory factor (LIF) in postnatal neuronal development by using ORNs as a model. LIF is a multifunctional cytokine implicated in various aspects of neuronal development, including phenotype determination, survival, and in response to nerve injury. LIF-deficient mice display significant increases, both in the absolute amount and in the number of cells expressing olfactory marker protein, a marker of mature ORNs. The maturation of ORNs was significantly inhibited by LIF in vitro. LIF activated the STAT3 pathway in ORNs, and transfection of ORNs with a dominant negative form of STAT3 abolished the effect of LIF. These findings demonstrate that LIF negatively regulates ORN maturation via the STAT3 pathway. Thus, LIF plays a critical role in controlling the transition of ORNs to maturity. Consequently, a population of ORNs is maintained in an immature state to facilitate the rapid repopulation of the olfactory epithelium with mature neurons during normal cell turnover or after injury