Texture-specific Si isotope variations in Barberton Greenstone Belt cherts record low temperature fractionations in early Archean seawater

Sedimentary cherts are unusually abundant in early Archean (pre-3.0 Ga) sequences, suggesting a silica cycle that was profoundly different than the modern system. Previously applied for the purpose of paleothermometry, Si isotopes in ancient cherts can offer broader insight into mass fluxes and mechanisms associated with silica concentration, precipitation, diagenesis, and metamorphism. Early Archean cherts contain a rich suite of sedimentological and petrographic textures that document a history of silica deposition, cementation, silicification, and recrystallization. To add a new layer of insight into the chemistry of early cherts, we have used wavelength-dispersive spectroscopy and then secondary ion mass spectrometry (SIMS) to produce elemental and Si and O isotope ratio data from banded black-and-white cherts from the Onverwacht Group of the Barberton Greenstone Belt, South Africa. This geochemical data is then interpreted in the framework of depositional and diagenetic timing of silica precipitation provided by geological observations. SIMS allows the comparison of Si and O isotope ratios of distinct silica phases, including black carbonaceous chert beds and bands (many including well-defined sedimentary grains), white relatively pure chert bands including primary silica granules, early cavity-filling cements, and later quartz-filled veins. Including all chert types and textures analyzed, the δ^(30)Si dataset spans a range from −4.78‰ to +3.74‰, with overall mean 0.20‰, median 0.51‰, and standard deviation 1.30‰ (n = 1087). Most samples have broadly similar δ^(30)Si distributions, but systematic texture-specific δ^(30)Si differences are observed between white chert bands (mean +0.60‰, n = 750), which contain textures that represent primary and earliest diagenetic silica phases, and later cavity-filling cements (mean −1.41‰, n = 198). We observed variations at a ∼100 μm scale indicating a lack of Si isotope homogenization at this scale during diagenesis and metamorphism, although fractionations during diagenetic phase transformations may have affected certain textures. We interpret these systematic variations to reflect fractionation during silica precipitation as well as isotopically distinct fluids from which later phases originated. SIMS δ^(18)O values fall in a range from 16.39‰ to 23.39‰ (n = 381), similar to previously published data from bulk gas source mass spectrometry of Onverwacht cherts. We observed only limited examples of texture-related variation in δ^(18)O and did not observe correlation of δ^(18)O with δ^(30)Si trends. This is consistent with hypotheses that Si isotope ratios are more resistant to alteration under conditions of rock-buffered diagenesis (Marin-Carbonne et al., 2011). Our results indicate that low temperature processes fractionated silicon isotopes in early Archean marine basins, a behavior that probably precludes the application of chert δ^(30)Si as a robust paleothermometer. The values we observe for facies that sedimentological and petrographic observations indicate formed as primary and earliest diagenetic silica precipitates from seawater are more ^(30)Si-rich than that expected for bulk silicate Earth. This is consistent with the hypothesis that the silicon isotope budget is balanced by the coeval deposition of ^(30)Si-enriched cherts and ^(30)Si-depleted iron formation lithologies. Precipitation of authigenic clay minerals in both terrestrial and marine settings may have also comprised a large ^(30)Si-depleted sink, with the corollary of an important non-carbonate alkalinity sink consuming cations released by silicate weathering

Modification of the visual response properties of cerebellar neurons by norepinephrine

Extracellular recordings were conducted in the paraflocculus of anesthetized Long-Evans pigmented rats to determine how iontophoresis of norepinephrine (NE) affects the responsiveness of individual Purkinje cells and interneurons to presentations of visual stimuli within their visual receptive fields. Presentations of moving or stationary visual stimuli during the control (pre-NE) period elicited simple spike excitations or inhibitory responses in slightly more than one-half (55%, n = 32) of the cells tested (20 of 38 Purkinje cells, 12 of 20 interneurons). The predominant effect of NE iontophoresis was to improve visually evoked responses in those neurons which showed modulations in their simple spike discharge to control presentations of visual stimuli. A clear enhancement of visual responses by NE (i.e., absolute increase over control) was observed in 18 of the units, and in 12 of the 14 remaining cells, reductions in stimulus-bound discharge during catecholamine iontophoresis were accompanied by much larger depressions in background activity, resulting in a net enhancement in the ratio of signal-to-noise. NE differentially affected responses to stimulus movement in the preferred and non-preferred direction in one-third of these neurons, such that directional selectivity was increased. However, the orientation bias of individual units was unchanged by NE. Iontophoretic application of the [beta]-adrenergic antagonist sotalol but not the [alpha]-adrenergic antagonist phentolamine blocked these facilitating noradrenergic effects. An additional feature of noradrenergic action was revealed in tests conducted in 26 cells which did not respond to control presentations of visual stimuli. Iontophoresis of NE resulted in the elicitation of visual responses in 11 of these units, suggesting the possibility that NE might act in some cases to gate the efficacy of subliminal synaptic input conveyed by classical afferent channels. It is proposed that an important aspect of noradrenergic action within local cerebellar circuits might be to refine the receptive field properties of individual neuronal elements and thereby improve information flow through the cerebellum.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28612/1/0000424.pd

Anticipation of pain enhances the nociceptive transmission and functional connectivity within pain network in rats

<p>Abstract</p> <p>Background</p> <p>Expectation is a very potent pain modulator in both humans and animals. There is evidence that pain transmission neurons are modulated by expectation preceding painful stimuli. Nonetheless, few studies have examined the influence of pain expectation on the pain-related neuronal activity and the functional connectivity within the central nociceptive network.</p> <p>Results</p> <p>This study used a tone-laser conditioning paradigm to establish the pain expectation in rats, and simultaneously recorded the anterior cingulate cortex (ACC), the medial dorsal thalamus (MD), and the primary somatosensory cortex (SI) to investigate the effect of pain expectation on laser-induced neuronal responses. Cross-correlation and partial directed coherence analysis were used to determine the functional interactions within and between the recorded areas during nociceptive transmission. The results showed that under anticipation condition, the neuronal activity to the auditory cue was significantly increased in the ACC area, whereas those to actual noxious stimuli were enhanced in all the recorded areas. Furthermore, neuronal correlations within and between these areas were significantly increased under conditions of expectation compared to those under non-expectation conditions, indicating an enhanced synchronization of neural activity within the pain network. In addition, information flow from the medial (ACC and MD) to the lateral (SI cortex) pain pathway increased, suggesting that the emotion-related neural circuits may modulate the neuronal activity in the somatosensory pathway during nociceptive transmission.</p> <p>Conclusion</p> <p>These results demonstrate that the nociceptive processing in both medial and lateral pain systems is modulated by the expectation of pain.</p

Morphine modulation of pain processing in medial and lateral pain pathways

<p>Abstract</p> <p>Background</p> <p>Despite the wide-spread use of morphine and related opioid agonists in clinic and their powerful analgesic effects, our understanding of the neural mechanisms underlying opioid analgesia at supraspinal levels is quite limited. The present study was designed to investigate the modulative effect of morphine on nociceptive processing in the medial and lateral pain pathways using a multiple single-unit recording technique. Pain evoked neuronal activities were simultaneously recorded from the primary somatosensory cortex (SI), ventral posterolateral thalamus (VPL), anterior cingulate cortex (ACC), and medial dorsal thalamus (MD) with eight-wire microelectrode arrays in awake rats.</p> <p>Results</p> <p>The results showed that the noxious heat evoked responses of single neurons in all of the four areas were depressed after systemic injection of 5 mg/kg morphine. The depressive effects of morphine included (i) decreasing the neuronal response magnitude; (ii) reducing the fraction of responding neurons, and (iii) shortening the response duration. In addition, the capability of cortical and thalamic neural ensembles to discriminate noxious from innocuous stimuli was decreased by morphine within both pain pathways. Meanwhile, morphine suppressed the pain-evoked changes in the information flow from medial to lateral pathway and from cortex to thalamus. These effects were completely blocked by pre-treatment with the opiate receptor antagonist naloxone.</p> <p>Conclusion</p> <p>These results suggest that morphine exerts analgesic effects through suppressing both sensory and affective dimensions of pain.</p

Ensemble encoding of nociceptive stimulus intensity in the rat medial and lateral pain systems

<p>Abstract</p> <p>Background</p> <p>The ability to encode noxious stimulus intensity is essential for the neural processing of pain perception. It is well accepted that the intensity information is transmitted within both sensory and affective pathways. However, it remains unclear what the encoding patterns are in the thalamocortical brain regions, and whether the dual pain systems share similar responsibility in intensity coding.</p> <p>Results</p> <p>Multichannel single-unit recordings were used to investigate the activity of individual neurons and neuronal ensembles in the rat brain following the application of noxious laser stimuli of increasing intensity to the hindpaw. Four brain regions were monitored, including two within the lateral sensory pain pathway, namely, the ventral posterior lateral thalamic nuclei and the primary somatosensory cortex, and two in the medial pathway, namely, the medial dorsal thalamic nuclei and the anterior cingulate cortex. Neuron number, firing rate, and ensemble spike count codings were examined in this study. Our results showed that the noxious laser stimulation evoked double-peak responses in all recorded brain regions. Significant correlations were found between the laser intensity and the number of responsive neurons, the firing rates, as well as the mass spike counts (MSCs). MSC coding was generally more efficient than the other two methods. Moreover, the coding capacities of neurons in the two pathways were comparable.</p> <p>Conclusion</p> <p>This study demonstrated the collective contribution of medial and lateral pathway neurons to the noxious intensity coding. Additionally, we provide evidence that ensemble spike count may be the most reliable method for coding pain intensity in the brain.</p

Factors Mediating Alcohol Craving and Relapse: Stress, Compulsivity, and Genetics

This article represents the proceedings of a symposium at the 2004 annual meeting of the International Society for Biomedical Research on Alcoholism in Heidelberg, Germany. The symposium was organized by Zachary A. Rodd and Giancarlo Colombo. The presentations were (1) Pharmacological reversal of cycled withdrawal-sensitized or stress-sensitized withdrawal anxiety and enhanced ethanol drinking, by Darin J. Knapp and George R. Breese, (2) Alcohol craving and relapse in rats genetically selected for high alcohol preference, by Zachary A. Rodd and Richard L. Bell, (3) Exposure to stress increases dopaminergic burst firing in awake rats, by Kristin Anstrom and Donald J. Woodward, (4) Involvement of cannabinoid CB1 and GABAB receptors in the control of relapse-like drinking in alcohol-preferring Sardinian alcohol-preferring rats by Giancarlo Colombo and Salvatore Serra, and (5) Stress-induced ethanol drinking in CB1−/−, POMC, and PENK knockout mice, by Idiko Racz and Andreas Zimmer

FORUM: Ecological networks: the missing links in biomonitoring science.

Monitoring anthropogenic impacts is essential for managing and conserving ecosystems, yet current biomonitoring approaches lack the tools required to deal with the effects of stressors on species and their interactions in complex natural systems.Ecological networks (trophic or mutualistic) can offer new insights into ecosystem degradation, adding value to current taxonomically constrained schemes. We highlight some examples to show how new network approaches can be used to interpret ecological responses.Synthesis and applications. Augmenting routine biomonitoring data with interaction data derived from the literature, complemented with ground-truthed data from direct observations where feasible, allows us to begin to characterise large numbers of ecological networks across environmental gradients. This process can be accelerated by adopting emerging technologies and novel analytical approaches, enabling biomonitoring to move beyond simple pass/fail schemes and to address the many ecological responses that can only be understood from a network-based perspective

Laboratory-based evaluation of legionellosis epidemiology in Ontario, Canada, 1978 to 2006

BACKGROUND: Legionellosis is a common cause of severe community acquired pneumonia and respiratory disease outbreaks. The Ontario Public Health Laboratory (OPHL) has conducted most testing for Legionella species in the Canadian province of Ontario since 1978, and represents a multi-decade repository of population-based data on legionellosis epidemiology. We sought to provide a laboratory-based review of the epidemiology of legionellosis in Ontario over the past 3 decades, with a focus on changing rates of disease and species associated with legionellosis during that time period. METHODS: We analyzed cases that were submitted and tested positive for legionellosis from 1978 to 2006 using Poisson regression models incorporating temporal, spatial, and demographic covariates. Predictors of infection with culture-confirmed L. pneumophila serogroup 1 (LP1) were evaluated with logistic regression models. Results: 1,401 cases of legionellosis tested positive from 1978 to 2006. As in other studies, we found a late summer to early autumn seasonality in disease occurrence with disease risk increasing with age and in males. In contrast to other studies, we found a decreasing trend in cases in the recent decade (IRR 0.93, 95% CI 0.91 to 0.95, P-value = 0.001); only 66% of culture-confirmed isolates were found to be LP1. CONCLUSION: Despite similarities with disease epidemiology in other regions, legionellosis appears to have declined in the past decade in Ontario, in contrast to trends observed in the United States and parts of Europe. Furthermore, a different range of Legionella species is responsible for illness, suggesting a distinctive legionellosis epidemiology in this North American region