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Cluster Density (cluster + density)

Distribution by Scientific Domains

Medical Sciences	60%

Selected Abstracts

Sorbitol and myo -inositol levels and morphology of sural nerve in relation to peripheral nerve function and clinical neuropathy in men with diabetic, impaired, and normal glucose tolerance

DIABETIC MEDICINE, Issue 4 2000
G. Sundkvist
Abstracts Aims Sorbitol and myo -inositol levels and morphology of sural nerve were compared with nerve function and clinical neuropathy in men with diabetic, impaired (IGT), and normal glucose tolerance. Methods After neurography of sural nerve and determinations of sensory thresholds for vibration, warm and cold on the foot, whole nerve sural nerve biopsy was performed in 10 men with Type 1 diabetes mellitus, 10 with IGT, and 10 with normal glucose tolerance. Polyol levels were assessed by gas,liquid chromatography/mass spectrometry. Results Sural nerve amplitudes were significantly lower and sorbitol levels significantly higher in diabetic patients (median (interquartile range)) (3.7 (3.5) ,V and 643 (412) pmol/mg protein, respectively) both compared with IGT (11.3 (10.6) ,V; P = 0.04 and 286 (83) pmol/mg protein; P = 0.0032, respectively) and normally glucose tolerant (10.0 (11.6); P = 0.0142 and 296 (250) pmol/mg protein; P = 0.0191, respectively) subjects. There were no differences in nerve morphology between the three groups. Nerve myo -inositol levels correlated, however, positively with cluster density (rs = 0.56; P = 0.0054). In diabetic and IGT subjects, sural nerve amplitudes (2.6 (3.8) vs. 12.1 (10.6) ,V; P = 0.0246) and myelinated nerve fibre density (MNFD; 4076 (1091) vs. 5219 (668) nerve fibres/mm2; P = 0.0021) were significantly lower in nine subjects with clinical neuropathy than in 10 without. Conclusions Nerve degeneration (i.e. MNFD) correlated with clinical neuropathy but not with glucose tolerance status whereas nerve myo -inositol levels positively correlated with signs of nerve regeneration (i.e. increased cluster density). [source]

Organization of GABAA receptor ,-subunit clustering in the developing rat neocortex and hippocampus

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2004
B. Hutcheon
Abstract We compared the expression and co-expression of ,1, ,2, ,3, and ,5-subunit protein clusters of the ,-aminobutyric acid (GABA)A receptor in the neocortex and hippocampus of rat at postnatal days (PND) 5,10 and 30,40 in order to understand how inhibitory receptors reorganize during brain maturation. The size, intensity, density and pattern of co-localization of fluorescently tagged subunit clusters were determined in deconvolved digital images using a novel 2D cross-correlational analysis. The cross-correlation analysis allowed an unbiased identification of GABAA receptor subunit clusters based on staining intensity. Cluster size increased through development; only the ,2 clusters in dentate gyrus (DG) decreased in size. ,5-subunit cluster density either increased or decreased with maturation depending on the brain region. For the other subunits, the cluster density remained rather constant, with noted exceptions (increase in ,2 clusters in cortical layer 5 but a decrease of ,3 clusters in hilus). The co-localization of ,1-subunit with the others was unique and not correlated to overall changes in subunit abundance between developmental époques. So, although ,2-subunit expression went up in the DG, the clusters became less co-localized with ,1. In contrast, ,5-subunit clusters became more co-localized with ,1 as the ,5-subunit expression declined in cortex and CA1. The co-localization of ,3 with ,1 also became greater in layer 6. In the adult brain not all clustering was associated with synapses, as many ,-subunit clusters did not co-localize with synaptophysin. Overall, these data indicate that the regulation of GABAA receptor clustering is both synaptic and extrasynaptic, presumably reflecting complex cellular trafficking mechanisms. [source]

Cannabinoid receptor 1 signalling dampens activity and mitochondrial transport in networks of enteric neurones

NEUROGASTROENTEROLOGY & MOTILITY, Issue 9 2009
W. Boesmans
Abstract, Cannabinoid (CB) receptors are expressed in the enteric nervous system (ENS) and CB1 receptor activity slows down motility and delays gastric emptying. This receptor system has become an important target for GI-related drug development such as in obesity treatment. The aim of the study was to investigate how CB1 ligands and antagonists affect ongoing activity in enteric neurone networks, modulate synaptic vesicle cycling and influence mitochondrial transport in nerve processes. Primary cultures of guinea-pig myenteric neurones were loaded with different fluorescent markers: Fluo-4 to measure network activity, FM1-43 to image synaptic vesicles and Mitotracker green to label mitochondria. Synaptic vesicle cluster density was assessed by immunohistochemistry and expression of CB1 receptors was confirmed by RT-PCR. Spontaneous network activity, displayed by both excitatory and inhibitory neurones, was significantly increased by CB1 receptor antagonists (AM-251 and SR141716), abolished by CB1 activation (methanandamide, mAEA) and reduced by two different inhibitors (arachidonylamide serotonin, AA-5HT and URB597) of fatty acid amide hydrolase. Antagonists reduced the number of synaptic vesicles that were recycled during an electrical stimulus. CB1 agonists (mAEA and WIN55,212) reduced and antagonists enhanced the fraction of transported mitochondria in enteric nerve fibres. We found immunohistochemical evidence for an enhancement of synaptophysin-positive release sites with SR141716, while WIN55,212 caused a reduction. The opposite effects of agonists and antagonists suggest that enteric nerve signalling is under the permanent control of CB1 receptor activity. Using inhibitors of the endocannabinoid degrading enzyme, we were able to show there is endogenous production of a CB ligand in the ENS. [source]

Influence of non-random incorporation of Mn ions on the magnetotransport properties of Ga1,xMnxAs alloys

PHYSICA STATUS SOLIDI (C) - CURRENT TOPICS IN SOLID STATE PHYSICS, Issue 3 2008
C. Michel
Abstract We study theoretically the influence of a spatially nonrandom incorporation of Mn ions on the magnetotransport in paramagnetic Ga1,xMnxAs alloys. Such a nonrandomness may be introduced during post-growth annealing treatment. We use a resistor-network model for describing the electrical transport of this disordered semiconductor system as a function of temperature and external magnetic field. The model is founded on classical semiconductor band-transport and neglects many-body interactions. The peculiarities of paramagnetic dilute magnetic semiconductors, in particular, the magnetic-field induced changes of the density of states, the broad acceptor-energy distribution, and the interplay of magnetic field independent disorder (due to the alloying of GaAs with Mn) and magnetic field dependent disorder (due to the the Giant Zeeman splitting) are accounted for in a mean-field fashion. We have previously shown that this empirical transport model based on reasonable assumptions and realistic material parameters yields a satisfactory quantitative description of the experimentally obtained temperature and magnetic-field dependence of the resistivity of Ga0.98Mn0.02As samples annealed at different temperatures. For Ga1,xMnxAs alloys annealed at temperatures above 500 °C where structural changes lead to the formation of MnAs clusters, the transport is dominated by the paramagnetic GaAs:Mn host matrix as the cluster density is below the percolation threshold. We will show that in this situation the transport results can only be explained accounting for a nonrandom Mn distribution. Thus the analysis shown here provides further understanding of the annealing-induced changes of the transport properties in dilute magnetic III-Mn-V semiconductors. (© 2008 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [source]

AMPA receptor antibodies in limbic encephalitis alter synaptic receptor location,

ANNALS OF NEUROLOGY, Issue 4 2009
Meizan Lai MD
Objective To report the clinical and immunological features of a novel autoantigen related to limbic encephalitis (LE) and the effect of patients' antibodies on neuronal cultures. Methods We conducted clinical analyses of 10 patients with LE. Immunoprecipitation and mass spectrometry were used to identify the antigens. Human embryonic kidney 293 cells expressing the antigens were used in immunocytochemistry and enzyme-linked immunoabsorption assay. The effect of patients' antibodies on cultures of live rat hippocampal neurons was determined with confocal microscopy. Results Median age was 60 (38,87) years; 9 were women. Seven had tumors of the lung, breast, or thymus. Nine patients responded to immunotherapy or oncological therapy, but neurological relapses, without tumor recurrence, were frequent and influenced the long-term outcome. One untreated patient died of LE. All patients had antibodies against neuronal cell surface antigens that by immunoprecipitation were found to be the glutamate receptor 1 (GluR1) and GluR2 subunits of the ,-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR). Human embryonic kidney 293 cells expressing GluR1/2 reacted with all patients' sera or cerebrospinal fluid, providing a diagnostic test for the disorder. Application of antibodies to cultures of neurons significantly decreased the number of GluR2-containing AMPAR clusters at synapses with a smaller decrease in overall AMPAR cluster density; these effects were reversed after antibody removal. Interpretation Antibodies to GluR1/2 associate with LE that is often paraneoplastic, treatment responsive, and has a tendency to relapse. Our findings support an antibody-mediated pathogenesis in which patients' antibodies alter the synaptic localization and number of AMPARs. Ann Neurol 2009;65:424,434 [source]