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  • American Physiological Society  (6)
  • 2005-2009  (6)
Type of Medium
Publisher
  • American Physiological Society  (6)
Language
Years
  • 2005-2009  (6)
Year
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2009
    In:  Journal of Neurophysiology Vol. 101, No. 3 ( 2009-03), p. 1126-1140
    In: Journal of Neurophysiology, American Physiological Society, Vol. 101, No. 3 ( 2009-03), p. 1126-1140
    Abstract: The mechanisms underlying neuronal coding and, in particular, the role of temporal spike coordination are hotly debated. However, this debate is often confounded by an implicit discussion about the use of appropriate analysis methods. To avoid incorrect interpretation of data, the analysis of simultaneous spike trains for precise spike correlation needs to be properly adjusted to the features of the experimental spike trains. In particular, nonstationarity of the firing of individual neurons in time or across trials, a spike train structure deviating from Poisson, or a co-occurrence of such features in parallel spike trains are potent generators of false positives. Problems can be avoided by including these features in the null hypothesis of the significance test. In this context, the use of surrogate data becomes increasingly important, because the complexity of the data typically prevents analytical solutions. This review provides an overview of the potential obstacles in the correlation analysis of parallel spike data and possible routes to overcome them. The discussion is illustrated at every stage of the argument by referring to a specific analysis tool (the Unitary Events method). The conclusions, however, are of a general nature and hold for other analysis techniques. Thorough testing and calibration of analysis tools and the impact of potentially erroneous preprocessing stages are emphasized.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Cell Physiology Vol. 293, No. 5 ( 2007-11), p. C1481-C1488
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 293, No. 5 ( 2007-11), p. C1481-C1488
    Abstract: The growing worldwide obesity epidemic is frequently linked to an increased risk of developing diseases such as diabetes, cardiovascular disease, and cancer. These diseases are associated with the infiltration of macrophages in white adipose tissue (WAT), the artery wall, and tumors, respectively; and these macrophages likely contribute to disease progression and pathogenesis. Abdominal WAT, adipose tissue surrounding the heart and artery wall, as well as carcinoma cells, secrete many factors that could induce macrophage infiltration. Leptin is an adipocyte-secreted hormone, and deficiency of either leptin or its receptor has been shown to cause morbid obesity in animals and in humans. However, what is more commonly noted in human obesity is the presence of central leptin resistance leading to hyperleptinemia. As leptin receptors are present on macrophages, we hypothesized that leptin could act as a monocyte/macrophage chemoattractant. Our current study demonstrates: 1) leptin is a potent chemoattractant for monocytes and macrophages, inducing maximal chemotactic responses at 1 ng/ml; 2) leptin-mediated chemotaxis requires the presence of full-length leptin receptors on migrating cells; 3) leptin causes increased influx of intracellular calcium in macrophages; and 4) activation of janus kinase/signal transducers and activators of transduction (JAK/STAT), mitogen-activated protein kinase (MAPK), and phosphatidylinositol 3-kinase (PI3K) pathways are all necessary for leptin-induced macrophage migration. Taken together, these data demonstrate that leptin is a potent monocyte/macrophage chemoattractant in vitro and that canonical cell motility machinery is activated upon macrophage exposure to leptin. These data have implications for the impact of hyperleptinemia on obesity-related pathophysiological conditions such as diabetes, cardiovascular disease, and cancer.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 2008
    In:  Journal of Neurophysiology Vol. 100, No. 3 ( 2008-09), p. 1523-1532
    In: Journal of Neurophysiology, American Physiological Society, Vol. 100, No. 3 ( 2008-09), p. 1523-1532
    Abstract: When inspecting visual scenes, primates perform on average four saccadic eye movements per second, which implies that scene segmentation, feature binding, and identification of image components is accomplished in 〈 200 ms. Thus individual neurons can contribute only a small number of discharges for these complex computations, suggesting that information is encoded not only in the discharge rate but also in the timing of action potentials. While monkeys inspected natural scenes we registered, with multielectrodes from primary visual cortex, the discharges of simultaneously recorded neurons. Relating these signals to eye movements revealed that discharge rates peaked around 90 ms after fixation onset and then decreased to near baseline levels within 200 ms. Unitary event analysis revealed that preceding this increase in firing there was an episode of enhanced response synchronization during which discharges of spatially distributed cells coincided within 5-ms windows significantly more often than predicted by the discharge rates. This episode started 30 ms after fixation onset and ended by the time discharge rates had reached their maximum. When the animals scanned a blank screen a small change in firing rate, but no excess synchronization, was observed. The short latency of the stimulation-related synchronization phenomena suggests a fast-acting mechanism for the coordination of spike timing that may contribute to the basic operations of scene segmentation.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 294, No. 3 ( 2008-03), p. E488-E495
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 294, No. 3 ( 2008-03), p. E488-E495
    Abstract: Plasma leptin is often elevated in obese individuals, and previous studies have suggested leptin as a factor that links obesity and atherosclerosis. Because macrophages play a key role in atherogenesis and are responsive to leptin, we hypothesized that leptin increases aortic root lesion formation, in part, through macrophage leptin receptor (LepR). Three different bone marrow transplantation studies were conducted in which bone marrow, with or without LepR, was transplanted into lethally irradiated 1) LDL receptor-deficient (LDLR −/− ) mice with moderate hyperleptinemia due to Western diet (WD) feeding, 2) LDLR −/− mice with WD feeding plus pharmacologically induced hyperleptinemia (daily injection of 125 μg leptin), or 3) obese, hyperleptinemic, LepR-deficient LDLR −/− (LepR db/db ;LDLR −/− ) mice. Minor differences in plasma parameters such as cholesterol, triglycerides, and insulin were observed in some groups; however, a consistent trend for the role of LepR on these parameters was not detected. In each of the studies, macrophage LepR expression did not have an effect on aortic root atherosclerotic lesion formation. These results suggest that nonhematopoietic cells may have a more significant role than macrophages in leptin-mediated effects on aortic root lesion formation.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 2008
    In:  Journal of Neurophysiology Vol. 100, No. 4 ( 2008-10), p. 2165-2176
    In: Journal of Neurophysiology, American Physiological Society, Vol. 100, No. 4 ( 2008-10), p. 2165-2176
    Abstract: The synfire chain model has been proposed as the substrate that underlies computational processes in the brain and has received extensive theoretical study. In this model cortical tissue is composed of a superposition of feedforward subnetworks (chains) each capable of transmitting packets of synchronized spikes with high reliability. Computations are then carried out by interactions of these chains. Experimental evidence for synfire chains has so far been limited to inference from detection of a few repeating spatiotemporal neuronal firing patterns in multiple single-unit recordings. Demonstration that such patterns actually come from synfire activity would require finding a meta organization among many detected patterns, as yet an untried approach. In contrast we present here a new method that directly visualizes the repetitive occurrence of synfire activity even in very large data sets of multiple single-unit recordings. We achieve reliability and sensitivity by appropriately averaging over neuron space (identities) and time. We test the method with data from a large-scale balanced recurrent network simulation containing 50 randomly activated synfire chains. The sensitivity is high enough to detect synfire chain activity in simultaneous single-unit recordings of 100 to 200 neurons from such data, enabling application to experimental data in the near future.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 294, No. 2 ( 2008-02), p. E284-E290
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 294, No. 2 ( 2008-02), p. E284-E290
    Abstract: Previous studies have demonstrated that macrophage-derived apolipoprotein E (apoE) reduces atherosclerotic lesion formation in lean apoE-deficient ( −/− ) mice. apoE has also been demonstrated to play a role in adipocyte differentiation and lipid accumulation. Because the prevalence of obesity has grown to epidemic proportions, we sought to determine whether macrophage-derived apoE could impact atherosclerotic lesion formation or adipose tissue expansion and inflammation in obese apoE −/− mice. To this end, we transplanted obese leptin-deficient ( ob/ ob) apoE −/− mice with bone marrow from either ob/ ob;apoE −/− or ob/ ob;apoE +/+ donors. There were no differences in body weight, total body adipose tissue, or visceral fat pad mass between recipient groups. The presence of macrophage-apoE had no impact on adipose tissue macrophage content or inflammatory cytokine expression. Recipients of apoE +/+ marrow demonstrated 3.7-fold lower plasma cholesterol ( P 〈 0.001) and 1.7-fold lower plasma triglyceride levels ( P 〈 0.01) by 12 wk after transplantation even though apoE was present in plasma at concentrations 〈 10% of wild-type levels. The reduced plasma lipids reflected a dramatic decrease in very low density lipoprotein and a mild increase in high-density lipoprotein levels. Atherosclerotic lesion area was 〉 10-fold lower in recipients of ob/ ob;apoE +/+ marrow ( P 〈 0.005). Similar results were seen in leptin receptor-deficient ( db/ db) apoE −/− mice. Finally, when bone marrow transplantation was performed in 4-mo-old ob/ ob;apoE −/− and db/ db;apoE −/− mice with preexisting lesions, recipients of apoE +/+ marrow had a 2.8-fold lower lesion area than controls ( P = 0.0002). These results demonstrate that macrophage-derived apoE does not impact adipose tissue expansion or inflammatory status; however, even very low levels of macrophage-derived apoE are capable of reducing plasma lipids and atherosclerotic lesion area in obese mice.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477331-4
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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