Subsea permafrost organic carbon stocks are large and of dominantly low reactivity.

Subsea permafrost carbon pools below the Arctic shelf seas are a major unknown in the global carbon cycle. We combine a numerical model of sedimentation and permafrost evolution with simplified carbon turnover to estimate accumulation and microbial decomposition of organic matter on the pan-Arctic shelf over the past four glacial cycles. We find that Arctic shelf permafrost is a globally important long-term carbon sink storing 2822 (1518-4982) Pg OC, double the amount stored in lowland permafrost. Although currently thawing, prior microbial decomposition and organic matter aging limit decomposition rates to less than 48 Tg OC/yr (25-85) constraining emissions due to thaw and suggesting that the large permafrost shelf carbon pool is largely insensitive to thaw. We identify an urgent need to reduce uncertainty in rates of microbial decomposition of organic matter in cold and saline subaquatic environments. Large emissions of methane more likely derive from older and deeper sources than from organic matter in thawing permafrost.

Thawing Yedoma permafrost is a neglected nitrous oxide source.

In contrast to the well-recognized permafrost carbon (C) feedback to climate change, the fate of permafrost nitrogen (N) after thaw is poorly understood. According to mounting evidence, part of the N liberated from permafrost may be released to the atmosphere as the strong greenhouse gas (GHG) nitrous oxide (N2O). Here, we report post-thaw N2O release from late Pleistocene permafrost deposits called Yedoma, which store a substantial part of permafrost C and N and are highly vulnerable to thaw. While freshly thawed, unvegetated Yedoma in disturbed areas emit little N2O, emissions increase within few years after stabilization, drying and revegetation with grasses to high rates (548 (133-6286) µg N m-2 day-1; median with (range)), exceeding by 1-2 orders of magnitude the typical rates from permafrost-affected soils. Using targeted metagenomics of key N cycling genes, we link the increase in in situ N2O emissions with structural changes of the microbial community responsible for N cycling. Our results highlight the importance of extra N availability from thawing Yedoma permafrost, causing a positive climate feedback from the Arctic in the form of N2O emissions.

Century-scale time since permafrost thaw affects temperature sensitivity of net methane production in thermokarst-lake and talik sediments.

Permafrost thaw subjects previously frozen soil organic carbon (SOC) to microbial degradation to the greenhouse gases carbon dioxide (CO2) and methane (CH4). Emission of these gases constitutes a positive feedback to climate warming. Among numerous uncertainties in estimating the strength of this permafrost carbon feedback (PCF), two are: (i) how mineralization of permafrost SOC thawed in saturated anaerobic conditions responds to changes in temperature and (ii) how microbial communities and temperature sensitivities change over time since thaw. To address these uncertainties, we utilized a thermokarst-lake sediment core as a natural chronosequence where SOC thawed and incubated in situ under saturated anaerobic conditions for up to 400 years following permafrost thaw. Initial microbial communities were characterized, and sediments were anaerobically incubated in the lab at four temperatures (0 °C, 3 °C, 10 °C, and 25 °C) bracketing those observed in the lake's talik. Net CH4 production in freshly-thawed sediments near the downward-expanding thaw boundary at the base of the talik were most sensitive to warming at the lower incubation temperatures (0 °C to 3 °C), while the overlying sediments which had been thawed for centuries had initial low abundant methanogenic communities (< 0.02%) and did not experience statistically significant increases in net CH4 production potentials until higher incubation temperatures (10 °C to 25 °C). We propose these observed differences in temperature sensitivities are due to differences in SOM quality and functional microbial community composition that evolve over time; however further research is necessary to better constrain the roles of these factors in determining temperature controls on anaerobic C mineralization.

Author Correction: Remote sensing quantifies widespread abundance of permafrost region disturbances across the Arctic and Subarctic.

The original version of this Article contained an error in the author affiliations. Affiliation 5 incorrectly read 'Tyumen State Oil and Gas University, Tyumen, Tyument. Oblast, Russian Federation, 625000'.This has now been corrected in both the PDF and HTML versions of the Article.

Remote sensing quantifies widespread abundance of permafrost region disturbances across the Arctic and Subarctic.

Local observations indicate that climate change and shifting disturbance regimes are causing permafrost degradation. However, the occurrence and distribution of permafrost region disturbances (PRDs) remain poorly resolved across the Arctic and Subarctic. Here we quantify the abundance and distribution of three primary PRDs using time-series analysis of 30-m resolution Landsat imagery from 1999 to 2014. Our dataset spans four continental-scale transects in North America and Eurasia, covering ~10% of the permafrost region. Lake area loss (-1.45%) dominated the study domain with enhanced losses occurring at the boundary between discontinuous and continuous permafrost regions. Fires were the most extensive PRD across boreal regions (6.59%), but in tundra regions (0.63%) limited to Alaska. Retrogressive thaw slumps were abundant but highly localized (<10-5%). Our analysis synergizes the global-scale importance of PRDs. The findings highlight the need to include PRDs in next-generation land surface models to project the permafrost carbon feedback.

Circumpolar distribution and carbon storage of thermokarst landscapes.

Thermokarst is the process whereby the thawing of ice-rich permafrost ground causes land subsidence, resulting in development of distinctive landforms. Accelerated thermokarst due to climate change will damage infrastructure, but also impact hydrology, ecology and biogeochemistry. Here, we present a circumpolar assessment of the distribution of thermokarst landscapes, defined as landscapes comprised of current thermokarst landforms and areas susceptible to future thermokarst development. At 3.6 × 106 km2, thermokarst landscapes are estimated to cover ∼20% of the northern permafrost region, with approximately equal contributions from three landscape types where characteristic wetland, lake and hillslope thermokarst landforms occur. We estimate that approximately half of the below-ground organic carbon within the study region is stored in thermokarst landscapes. Our results highlight the importance of explicitly considering thermokarst when assessing impacts of climate change, including future landscape greenhouse gas emissions, and provide a means for assessing such impacts at the circumpolar scale.

A simplified, data-constrained approach to estimate the permafrost carbon-climate feedback.

We present an approach to estimate the feedback from large-scale thawing of permafrost soils using a simplified, data-constrained model that combines three elements: soil carbon (C) maps and profiles to identify the distribution and type of C in permafrost soils; incubation experiments to quantify the rates of C lost after thaw; and models of soil thermal dynamics in response to climate warming. We call the approach the Permafrost Carbon Network Incubation-Panarctic Thermal scaling approach (PInc-PanTher). The approach assumes that C stocks do not decompose at all when frozen, but once thawed follow set decomposition trajectories as a function of soil temperature. The trajectories are determined according to a three-pool decomposition model fitted to incubation data using parameters specific to soil horizon types. We calculate litterfall C inputs required to maintain steady-state C balance for the current climate, and hold those inputs constant. Soil temperatures are taken from the soil thermal modules of ecosystem model simulations forced by a common set of future climate change anomalies under two warming scenarios over the period 2010 to 2100. Under a medium warming scenario (RCP4.5), the approach projects permafrost soil C losses of 12.2-33.4 Pg C; under a high warming scenario (RCP8.5), the approach projects C losses of 27.9-112.6 Pg C. Projected C losses are roughly linearly proportional to global temperature changes across the two scenarios. These results indicate a global sensitivity of frozen soil C to climate change (γ sensitivity) of -14 to -19 Pg C °C(-1) on a 100 year time scale. For CH4 emissions, our approach assumes a fixed saturated area and that increases in CH4 emissions are related to increased heterotrophic respiration in anoxic soil, yielding CH4 emission increases of 7% and 35% for the RCP4.5 and RCP8.5 scenarios, respectively, which add an additional greenhouse gas forcing of approximately 10-18%. The simplified approach presented here neglects many important processes that may amplify or mitigate C release from permafrost soils, but serves as a data-constrained estimate on the forced, large-scale permafrost C response to warming.

Climate change and the permafrost carbon feedback.

Large quantities of organic carbon are stored in frozen soils (permafrost) within Arctic and sub-Arctic regions. A warming climate can induce environmental changes that accelerate the microbial breakdown of organic carbon and the release of the greenhouse gases carbon dioxide and methane. This feedback can accelerate climate change, but the magnitude and timing of greenhouse gas emission from these regions and their impact on climate change remain uncertain. Here we find that current evidence suggests a gradual and prolonged release of greenhouse gas emissions in a warming climate and present a research strategy with which to target poorly understood aspects of permafrost carbon dynamics.

A shift of thermokarst lakes from carbon sources to sinks during the Holocene epoch.

Thermokarst lakes formed across vast regions of Siberia and Alaska during the last deglaciation and are thought to be a net source of atmospheric methane and carbon dioxide during the Holocene epoch. However, the same thermokarst lakes can also sequester carbon, and it remains uncertain whether carbon uptake by thermokarst lakes can offset their greenhouse gas emissions. Here we use field observations of Siberian permafrost exposures, radiocarbon dating and spatial analyses to quantify Holocene carbon stocks and fluxes in lake sediments overlying thawed Pleistocene-aged permafrost. We find that carbon accumulation in deep thermokarst-lake sediments since the last deglaciation is about 1.6 times larger than the mass of Pleistocene-aged permafrost carbon released as greenhouse gases when the lakes first formed. Although methane and carbon dioxide emissions following thaw lead to immediate radiative warming, carbon uptake in peat-rich sediments occurs over millennial timescales. We assess thermokarst-lake carbon feedbacks to climate with an atmospheric perturbation model and find that thermokarst basins switched from a net radiative warming to a net cooling climate effect about 5,000 years ago. High rates of Holocene carbon accumulation in 20 lake sediments (47 ± 10 grams of carbon per square metre per year; mean ± standard error) were driven by thermokarst erosion and deposition of terrestrial organic matter, by nutrient release from thawing permafrost that stimulated lake productivity and by slow decomposition in cold, anoxic lake bottoms. When lakes eventually drained, permafrost formation rapidly sequestered sediment carbon. Our estimate of about 160 petagrams of Holocene organic carbon in deep lake basins of Siberia and Alaska increases the circumpolar peat carbon pool estimate for permafrost regions by over 50 per cent (ref. 6). The carbon in perennially frozen drained lake sediments may become vulnerable to mineralization as permafrost disappears, potentially negating the climate stabilization provided by thermokarst lakes during the late Holocene.

Thermokarst lakes as a source of atmospheric CH4 during the last deglaciation.

Polar ice-core records suggest that an arctic or boreal source was responsible for more than 30% of the large increase in global atmospheric methane (CH4) concentration during deglacial climate warming; however, specific sources of that CH4 are still debated. Here we present an estimate of past CH4 flux during deglaciation from bubbling from thermokarst (thaw) lakes. Based on high rates of CH4 bubbling from contemporary arctic thermokarst lakes, high CH4 production potentials of organic matter from Pleistocene-aged frozen sediments, and estimates of the changing extent of these deposits as thermokarst lakes developed during deglaciation, we find that CH4 bubbling from newly forming thermokarst lakes comprised 33 to 87% of the high-latitude increase in atmospheric methane concentration and, in turn, contributed to the climate warming at the Pleistocene-Holocene transition.

Embryonic and postnatal development of the serotonergic raphe system and its target regions in 5-HT1A receptor deletion or overexpressing mouse mutants.

The neurotransmitter 5-HT regulates early developmental processes in the CNS. In the present study we followed the embryonic and postnatal development of serotonergic raphe neurons and catecholaminergic target systems in the brain of 5-HT1A receptor knockout (KO) and overexpressing (OE) in comparison with wild-type (WT) mice from embryonic day (E) 12.5 to postnatal day (P) 15.5. Up to P15.5 no differences were apparent in the differentiation and distribution of serotonergic neurons in the raphe area as revealed by the equal number of serotonergic neurons in the dorsal raphe in all three genotypes. However, the establishment of serotonergic projections to the mesencephalic tegmentum and hypothalamus was delayed at E12.5 in KO and OE animals and projections to the cerebral cortex between E16.5 and E18.5 were delayed in OE mice. This delay was only transient and did not occur in other brain areas including septum, hippocampus and striatum. Moreover, OE mice caught up with WT and KO animals postnatally such that at P1.5 serotonergic innervation of the cortex was more extensive in the OE than in KO and WT mice. Tissue levels of 5-HT and of its main metabolite 5-hydroxyindoleacetic acid as well as 5-HT turnover were considerably higher in brains of OE mice and slightly elevated in KO mice in comparison with the WT, starting at E16.5 through P15.5. The initial differentiation of dopaminergic neurons and fibers in the substantia nigra at E12.5 was transiently delayed in KO and OE mice as compared with WT mice, but no abnormalities in noradrenergic development were apparent in later stages. The present data indicate that 5-HT1A receptor deficiency or overexpression is associated with increased 5-HT synthesis and turnover in the early postnatal period. However, they also show that effects of 5-HT1A KO or OE on the structural development of the serotonergic system are at best subtle and transient. They may nonetheless contribute to the establishment of increased or reduced anxiety-like behavior, respectively, in adult mice.

Differential distribution of voltage-gated potassium channels Kv 1.1-Kv1.6 in the rat retina during development.

The discharge behavior of neurons depends on a variable expression and sorting pattern of voltage-dependent potassium (Kv) channels that changes during development. The rodent retina represents a neuronal network whose main functions develop after birth. To obtain information about neuronal maturation we analyzed the expression of subunits of the Kv1 subfamily in the rat retina during postnatal development using immunocytochemistry and immunoelectron microscopy. At postnatal day 5 (P5) all the alpha-subunits of Kv1.1-Kv1.6 channels were found to be expressed in the ganglion cell layer (GCL), most of them already at P1 or P3. Their expression upregulates postnatally and the pattern and distribution change in an isoform-specific manner. Additionally Kv1 channels are found in the outer and inner plexiform layer (OPL, IPL) and in the inner nuclear layer (INL) at different postnatal stages. In adult retina the Kv 1.3 channel localizes to the inner and outer segments of cones. In contrast, Kv1.4 is highly expressed in the outer retina at P8. In adult retina Kv1.4 occurs in rod inner segments (RIS) near the connecting cilium where it colocalizes with synapse associated protein SAP 97. By using confocal laser scanning microscopy we showed a differential localization of Kv1.1-1.6 to cholinergic amacrine and rod bipolar cells of the INL of the adult retina.

Effects of brain-derived neurotrophic factor (BDNF) on glial cells and serotonergic neurones during development.

Serotonergic neurones are among the first to develop in the central nervous system. Their survival and maturation is promoted by a variety of factors, including serotonin itself, brain-derived neurotrophic factor (BDNF) and S100beta, an astrocyte-specific Ca(2+) binding protein. Here, we used BDNF-deficient mice and cell cultures of embryonic raphe neurones to determine whether or not BDNF effects on developing serotonergic raphe neurones are influenced by its action on glial cells. In BDNF-/- mice, the number of serotonin-immunoreactive neuronal somata, the amount of the serotonin transporter, the serotonin content in the striatum and the hippocampus, and the content of 5-hydroxyindoleacetic acid in all brain regions analysed were increased. By contrast, reduced immunoreactivity was found for myelin basic protein (MBP) in all brain areas including the raphe and its target region, the hippocampus. Exogenously applied BDNF increased the number of MBP-immunopositive cells in the respective culture systems. The raphe area displayed selectively reduced immunoreactivity for S100beta. Accordingly, S100beta was increased in primary cultures of pure astrocytes by exogenous BDNF. In glia-free neuronal cultures prepared from the embryonic mouse raphe, addition of BDNF supported the survival of serotonergic neurones and increased the number of axon collaterals and primary dendrites. The latter effect was inhibited by the simultaneous addition of S100beta. These results suggest that the presence of BDNF is not a requirement for the survival and maturation of serotonergic neurones in vivo. BDNF is, however, required for the local expression of S100beta and production of MBP. Therefore BDNF might indirectly influence the development of the serotonergic system by stimulating the expression of S100beta in astrocytes and the production MBP in oligodendrocytes.

Differential effects of Rho GTPases on axonal and dendritic development in hippocampal neurones.

Formation of neurites and their differentiation into axons and dendrites requires precisely controlled changes in the cytoskeleton. While small GTPases of the Rho family appear to be involved in this regulation, it is still unclear how Rho function affects axonal and dendritic growth during development. Using hippocampal neurones at defined states of differentiation, we have dissected the function of RhoA in axonal and dendritic growth. Expression of a dominant negative RhoA variant inhibited axonal growth, whereas dendritic growth was promoted. The opposite phenotype was observed when a constitutively active RhoA variant was expressed. Inactivation of Rho by C3-catalysed ADP-ribosylation using C3 isoforms (Clostridium limosum, C3(lim) or Staphylococcus aureus, C3(stau2)), diminished axonal branching. By contrast, extracellularly applied nanomolar concentrations of C3 from C. botulinum (C3(bot)) or enzymatically dead C3(bot) significantly increased axon growth and axon branching. Taken together, axonal development requires activation of RhoA, whereas dendritic development benefits from its inactivation. However, extracellular application of enzymatically active or dead C3(bot) exclusively promotes axonal growth and branching suggesting a novel neurotrophic function of C3 that is independent from its enzymatic activity.

Deltamethrin differentially affects neuronal subtypes in hippocampal primary culture.

The effects of deltamethrin on neuronal development and survival were studied using primary mouse hippocampal neurons in culture. Repeated applications of deltamethrin (between 2 nM and 2000 nM) decreased the number of neurons by 16-40%, respectively. Neuronal death was accompanied by an overall decrease of synaptic proteins. Deltamethrin treatment increased the K(+)-stimulated release of amino acid transmitters, GABA and glutamate. The release of the latter might also contribute to neuronal damage. A considerable number of neurons survived treatment with high concentrations of deltamethrin (200-2000 nM) and still displayed characteristics of mature neurons such as synaptic contacts or the expression of members of the Kv1 channel family. When analyzing subtypes of neurons calbindin- as well as somatostatin-positive neurons decreased by 50% after repeated treatment with 2 nM deltamethrin. Under the same conditions neuropeptide Y-positive neurons were up-regulated by 250%.Taken together these data show that deltamethrin at concentrations relevant in human toxicology differentially affects survival of neuronal subtypes by exerting either deleterious or supportive effects. We conclude that deltamethrin disturbs fine-tuning of neuronal efficiency in neuronal networks and might also interfere with the correct wiring during development.

Filiform polyposis of the colon in chronic inflammatory bowel disease (so-called giant inflammatory polyps).

On the basis of 3 of our own cases, we describe unusually intense forms of filiform polyposis and local giant polyposis as a consequence of chronic inflammatory bowel disease. The patients are: A 52-year-old woman who for 7 years has been known to have Crohn's disease (CD); a 55-year-old man who for 14 years has been known to have chronic inflammatory bowel disease, which was first thought to have been ulcerative colitis, but, as a result of the findings on the subtotal colectomy specimen, had to be classified as Crohn's disease or colitis indeterminate; and a 53-year-old woman known to have had ulcerative colitis for 37 years. From the literature on the subject, we drew up a chronological list of a total of 43 cases with similar or completely identical findings. The clinical significance of the findings in their particularly massive intensity results from their necessary differentiation--in the context of differential diagnosis--from a malignant tumor, in particular from a carcinoma in association with chronic inflammatory bowel disease, or from a villous adenoma. The indication of a need to operate results from the impossibility of being able definitely to rule out a malignant degeneration by means of clinical methods. Also, experience shows that with massive findings of the kind described a spontaneous disappearance cannot be expected. Finally, too, the clinical symptoms and the patients subjective complaints necessitate balanced surgical treatment, taking into consideration the site and the extent of the lesion.

[Clinical behavior of serous and mucinous borderline tumors of the ovary with diploid DNA stem line. Follow-up studies after organ preserving and non-organ preserving therapy]. / Zum klinischen Verhalten von serösen und muzinösen Borderline-Tumoren des Ovars mit diploider DNA-Stammlinie. Verlaufsbeobachtungen nach organerhaltender und nicht-organerhaltender Therapie.

Even today, the situation is still unclear with regard to the radicality of the operation and any adjuvant therapy required in treatment of borderline tumors of the ovary. In the last two decades, treatment of these tumors in the Department of Gynecology and Obstetrics at our hospital has depended on the stage of the disease and the age of the patient. It ranged from laparoscopic cyst extirpation to hysterectomy with bilateral adnectomy and omental resection and regional lymphnodectomy. From the end of 1985 to the end of 1992, 35 patients with borderline tumors of the ovaries were operated on. Histologically, 14 borderline tumors were mucinous, 21 were serous. A follow-up investigation was carried out five to 11 years after primary operation. In this period, no patient died of borderline tumor. Twenty-eight patients who were followed up were clinically free of recurrence, five patients are alive, but could not be followed up. Two patients have died of other diseases after five years. Only one patient received adjuvant chemotherapy. She could not be followed up. In the meantime, peritoneal implants were demonstrated at second-look laparoscopies in four out of 18 patients. Later, these could no longer be demonstrated (one patient) or did not affect the survival time (three patients) and thus ultimately was not pathologically relevant. Primarily, two of these four patient had stage Ia-Ic. The paraffin blocks of the preparations are still available from 26 patients, and additional investigations could be carried out. Nineteen percent of the borderline tumors showed micropapillary structures of an MPCS (= micropapillary serous carcinoma), which evidently did not have a negative effect on the prognosis. All borderline tumors showed diploid distributions in DNA cytometry. It is not possible to make a definitive treatment recommendation on the basis of this investigation because the number of patients followed up was too small.

Expression of Kv1 potassium channels in mouse hippocampal primary cultures: development and activity-dependent regulation.

Excitability and discharge behavior of neurons depends on the highly variable expression pattern of voltage-dependent potassium (Kv) channels throughout the nervous system. To learn more about distribution, development, and activity-dependent regulation of Kv channel subunit expression in the rodent hippocampus, we studied the protein expression of members of the Kv1 subfamily in mouse hippocampus in situ and in primary cultures. In adult hippocampus, Kv1 (1-6) channel alpha-subunits were present, whereas at postnatal day 2, none of these proteins could be detected in CA1-CA3 and dentate gyrus. Kv1.1 was the first channel to be observed at postnatal day 6. The delayed postnatal expression and most of the subcellular distribution observed in hippocampal sections were mimicked by cultured hippocampal neurons in which Kv channels appeared only after 10 days in vitro. This developmental upregulation was paralleled by a dramatic increase in total K(+) current, as well as an elevated GABA release in the presence of 4-aminopyridine. Thus, the developmental profile, subcellular localization, and functionality of Kv1 channels in primary culture of hippocampus closely resembles the in situ situation. Impairing secretion by clostridial neurotoxins or blocking activity by tetrodotoxin inhibited the expression of Kv1.1, Kv1.2, and Kv1.4, whereas the other Kv1 channels still appeared. This activity-dependent depression was only observed before the initial appearance of the respective channels and lost after they had been expressed. Our data show that hippocampal neurons in culture are a convenient model to study the developmental expression and regulation of Kv1 channels. The ontogenetic regulation and the activity-dependent expression of Kv1.1, Kv1.2, and Kv1.4 indicate that neuronal activity plays a crucial role for the development of the mature Kv channel pattern in hippocampal neurons.

SNAP-25 requirement for dendritic growth of hippocampal neurons.

Structure and dimension of the dendritic arbor are important determinants of information processing by the nerve cell, but mechanisms and molecules involved in dendritic growth are essentially unknown. We investigated early mechanisms of dendritic growth using mouse fetal hippocampal neurons in primary culture, which form processes during the first week in vitro. We detected a key component of regulated exocytosis, SNAP-25 (synaptosomal associated protein of 25 kDa), in axons and axonal terminals as well as in dendrites identified by the occurrence of the dendritic markers transferrin receptor and MAP2. Selective inactivation of SNAP-25 by botulinum neurotoxin A (BoNTA) resulted in inhibition of axonal growth and of vesicle recycling in axonal terminals. In addition, dendritic growth of hippocampal pyramidal and granule neurons was significantly inhibited by BoNTA. In contrast, cleavage of synaptobrevin by tetanus toxin had an effect on neither axonal nor dendritic growth. Our observations indicate that SNAP-25, but not synaptobrevin, is involved in constitutive axonal growth and dendrite formation by hippocampal neurons.