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- Jankowska, Elzbieta, et al.
(författare)
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Contacts between serotoninergic fibres and dorsal horn spinocerebellar tract neurons in the cat and rat: A confocal microscopic study
- 1995
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Ingår i: Neuroscience. - 0306-4522. ; 67, s. 477-487
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Tidskriftsartikel (refereegranskat)abstract
- Contacts between serotoninergic nerve fibres and dorsal horn dorsal spinocerebellar tract neurons were analysed in order to investigate the morphological basis of actions of serotonin upon dorsal spinocerebellar tract neurons. In a series of experiments dorsal spinocerebellar tract neurons were labelled with intracellularly injected rhodamine-dextran in the cat. The neurons were monosynaptically excited by group II muscle afferents and cutaneous afferents and were identified by antidromic activation following stimuli applied in the cerebellum. In the second series of experiments dorsal spinocerebellar tract neurons were labelled by retrograde transport of Fluorogold injected into the cerebellum in the rat. In both series, serotoninergic fibres were labelled by using a specific anti-serotonin antiserum and were revealed by immunofluorescence. Appositions between the serotoninergic fibres and the cells were inspected with a dual channel confocal microscope. The merged images obtained with the two channels of the microscope were viewed in single optical planes 2 μm apart and in rotated three-dimensional reconstructions. Serotoninergic nerve fibres were found in apposition to cell bodies of all feline dorsal spinocerebellar tract neurons (n = 7) and of 75% of rat dorsal spinocerebellar tract neurons (n = 90). The numbers of putative contacts on cell bodies varied between less than 100 and nearly 300 (mean 160) in the cat and between about five and 30 in the rat. Contacts with dendrites of feline neurons were seen on 96% of 72 dendrites within 300 μm from soma and on 91% of 23 dendrites at distances of 300-500 μm. The number of such contacts varied from less than five to 150 on a single dendrite within these ranges of distances. Their total number within 100 μm from the soma was comparable or exceeded the number of contacts on the soma. © 1995 IBRO.
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| 2. |
- Belichenko, P V, et al.
(författare)
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Neuronal and fibre organization in neocortical grafts placed in post-ischaemic adult rat brain: a three-dimensional confocal microscopy study
- 2001
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Ingår i: Journal of Comparative Pathology. - : Elsevier BV. - 1532-3129 .- 0021-9975. ; 124:2-3, s. 142-148
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Tidskriftsartikel (refereegranskat)abstract
- The dendritic morphology in neocortical grafts was studied with three-dimensional confocal laser scanning microscopy after microinjection of Lucifer Yellow into individual cells. The grafts had been implanted into infarct cavities in the neocortex of hypertensive rats 46 weeks earlier. The carbocyanine dye method was used to identify afferent (host to transplant) and efferent (transplant to host) connections. Pyramidal, nonpyramidal and glial cells were present in the transplants. Some dendrites had an almost normal appearance, but abnormalities (atypical orientation of apical, basal or oblique apical dendrites) were observed. Some bi-apical pyramidal neurons and pyramidal neurons with obliquely oriented apical dendrites were also observed. Carbocyanine dye-labelled fibres of different diameter formed a dense network in the transplant, enabling the border between transplant and host tissue to be clearly recognized. No labelled fibres were observed to enter the host brain. Fibres with "boutons en passant" and no preferential orientation were noted. It is proposed that Lucifer Yellow microinjection may be a useful method in studies aimed at improving graft morphology. Failure to demonstrate host to transplant connections with the carbocyanine dye method was contrary to earlier studies in which tracers were applied in vivo. A combined use of in-vivo and post-mortem tracer techniques is needed to establish the reason for the discrepancy.
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| 3. |
- Peiris, Heshan, et al.
(författare)
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A Syntenic Cross Species Aneuploidy Genetic Screen Links RCAN1 Expression to β-Cell Mitochondrial Dysfunction in Type 2 Diabetes
- 2016
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Ingår i: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7390 .- 1553-7404. ; 12:5
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Tidskriftsartikel (refereegranskat)abstract
- Type 2 diabetes (T2D) is a complex metabolic disease associated with obesity, insulin resistance and hypoinsulinemia due to pancreatic β-cell dysfunction. Reduced mitochondrial function is thought to be central to β-cell dysfunction. Mitochondrial dysfunction and reduced insulin secretion are also observed in β-cells of humans with the most common human genetic disorder, Down syndrome (DS, Trisomy 21). To identify regions of chromosome 21 that may be associated with perturbed glucose homeostasis we profiled the glycaemic status of different DS mouse models. The Ts65Dn and Dp16 DS mouse lines were hyperglycemic, while Tc1 and Ts1Rhr mice were not, providing us with a region of chromosome 21 containing genes that cause hyperglycemia. We then examined whether any of these genes were upregulated in a set of ~5,000 gene expression changes we had identified in a large gene expression analysis of human T2D β-cells. This approach produced a single gene, RCAN1, as a candidate gene linking hyperglycemia and functional changes in T2D β-cells. Further investigations demonstrated that RCAN1 methylation is reduced in human T2D islets at multiple sites, correlating with increased expression. RCAN1 protein expression was also increased in db/db mouse islets and in human and mouse islets exposed to high glucose. Mice overexpressing RCAN1 had reduced in vivo glucose-stimulated insulin secretion and their β-cells displayed mitochondrial dysfunction including hyperpolarised membrane potential, reduced oxidative phosphorylation and low ATP production. This lack of β-cell ATP had functional consequences by negatively affecting both glucose-stimulated membrane depolarisation and ATP-dependent insulin granule exocytosis. Thus, from amongst the myriad of gene expression changes occurring in T2D β-cells where we had little knowledge of which changes cause β-cell dysfunction, we applied a trisomy 21 screening approach which linked RCAN1 to β-cell mitochondrial dysfunction in T2D.
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