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Träfflista för sökning "WFRF:(Tingström Anders) srt2:(2005-2009)"

Sökning: WFRF:(Tingström Anders) > (2005-2009)

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1.
  • Ekstrand, Joakim, et al. (författare)
  • Differential inhibition of neurogenesis and angiogenesis by corticosterone in rats stimulated with electroconvulsive seizures
  • 2008
  • Ingår i: Progress in Neuro-Psychopharmacology and Biological Psychiatry. - : Elsevier. - 0278-5846. ; 32:6, s. 1466-1472
  • Forskningsöversikt (refereegranskat)abstract
    • Antidepressant drugs and electroconvulsive seizure (ECS)-treatment, an animal model of electroconvulsive therapy, induce neurogenesis in adult rats. Stress and high levels of corticosterone (CORT) on the contrary inhibit neurogenesis. Hippocampal neurogenesis has been described to occur in an angiogenic niche where proliferation of neural progenitors takes place in an environment with active vascular growth. Here we investigate the effect of ECS-treatment on the proliferation of endothelial cells and neuronal precursors in hippocampus of CORT-treated rats. Bromodeoxyuridine (BrdU) was used to identify dividing cells. The number of newborn neuronal precursors and endothelial cells was quantified in the subgranular zone (SGZ) and the molecular layer (ML) of the dentate gyrus. The increase in neuronal precursor proliferation in the SGZ following ECS-treatment was not inhibited by elevated levels of CORT despite CORT strongly inhibiting ECS-induced endothelial cell proliferation. Also in the ML CORT-treatment inhibited the ECS-induced angiogenic response. We conclude that despite common factors regulating neurogenesis and angiogenesis, ECS-induced proliferation of neuronal precursors can take place even if the angiogenic response is blunted. Whether inhibition of angiogenesis affects other steps in the chain of events leading to the formation of fully integrated granule neurons remains to be elucidated. (C) 2008 Elsevier Inc. All rights reserved.
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2.
  • Ekstrand, Joakim, et al. (författare)
  • Environmental enrichment, exercise and corticosterone affect endothelial cell proliferation in adult rat hippocampus and prefrontal cortex.
  • 2008
  • Ingår i: Neuroscience Letters. - : Elsevier. - 0304-3940. ; 442, s. 203-207
  • Tidskriftsartikel (refereegranskat)abstract
    • Stress and environmental enrichment have opposing effects on cerebral cellular plasticity. Stress-induced disturbances in neuronal and glial plasticity have been implicated in the pathophysiology of affective disorders. Patients with depression often show volume reductions in specific brain regions. The mechanisms behind these changes are not well understood, but animal studies have indicated that increased levels of glucocorticoids and stress have negative impact on the neuronal and glial cell populations. On the contrary, enriched environment and physical activity have positive effects. In this study we have examined the effect of corticosterone (CORT), environmental enrichment (EE) and running on angiogenesis in hippocampus and prefrontal cortex (PFC). We demonstrate a dramatic inhibition in endothelial cell proliferation in these brain regions in CORT-treated rats. Environmental enrichment had the opposite effect and stimulated endothelial cell proliferation both in the hippocampus and in the PFC. Running had a stimulatory effect in hippocampus, but not in the PFC. We suggest that the angiostatic effect of CORT demonstrated in this study might be paralleled in human subjects exposed to high levels of stress hormones for prolonged periods of time. Raised cortisol levels in depressed or old patients could, by reducing endothelial cell formation/turnover, lead to rarefaction and aging of the vascular bed, and as a result, neuronal function could be impaired. It is tempting to speculate that a physically and intellectually active life may protect against stress-induced vascular changes. Therapeutic agents also targeting the cerebral vasculature could consequently constitute a new tool in the combat of stress-related disorders.
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3.
  • Hellsten, Johan, et al. (författare)
  • Electroconvulsive seizures induce angiogenesis in adult rat hippocampus
  • 2005
  • Ingår i: Biological Psychiatry. - : Elsevier. - 0006-3223. ; 58:11, s. 871-878
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Electroconvulsive seizure (ECS)-treatment, a model for electroconvulsive therapy (ECT) has been shown to induce proliferation of endothelial cells in the dentate gyrus (DG) of adult rats. Here we quantified the net angiogenic response after hypoxia a known inducer of aniogenesis. Therefore we also examined the effect of oxygenation on ECS-induced proliferation of endothelial cells. Methods: Total endothelial cell numbers and vessel length were estimated utilizing design based stereological analysis methods. Endothelial cell proliferation in the DG after ECS with or withouy oxygenation was assessed using bromodeoxyuridine. Results: The total number of endothelial cell numbers and vessels lenght was increased. Oxygenation did not abolish the ECS-induced proliferation of endothelial cells in the DG. Conclusions: ECS-treatment induces a dramatic increase in endothelial cell proliferation leading to a 30% increase in the total numberof endothelial cells. The increase in cell number resulted i na 16% increase in vessel length. These findings raise the possibility that similar vascular growth is induced by clinically administered ECT.
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5.
  • Jansson, Linda, et al. (författare)
  • Glial cell activation in response to electroconvulsive seizures
  • 2009
  • Ingår i: Progress in Neuro-Psychopharmacology and Biological Psychiatry. - : Elsevier. - 0278-5846. ; 33:7, s. 1119-1128
  • Forskningsöversikt (refereegranskat)abstract
    • Electroconvulsive therapy (ECT) is a very efficient treatment for severe depression. However, cognitive side effects have raised concern to whether ECT can cause cellular damage in vulnerable brain regions. A few recent animal studies have reported limited hippocampal cell loss, while a number of other studies have failed to find any signs of cellular damage and some even report that electroconvulsive seizures (ECS; the animal counterpart of ECT) has neuroprotective effects. We previously have described gliogenesis in response to ECS. Loss of glial cells is seen in depression and de novo formation of glial cells may thus have an important therapeutic role. Glial cell proliferation and activation is however also seen in response to neuronal damage. The aim of the present study was to further characterize glial cell activation in response to ECS. Two groups of rats were treated with 10 ECS using different sets of stimulus parameters. ECS-induced changes in the morphology and expression of markers typical for reactive microglia, astrocytes and NG2+ glial cells were analyzed immunohistochemically in prefrontal cortex, hippocampus, amygdala, hypothalamus, piriform cortex and entorhinal cortex. We observed changes in glial cell morphology and an enhanced expression of activation markers 2 h following ECS treatment, regardless of the stimulus parameters used. Four weeks later, few activated glial cells persisted. In conclusion, ECS treatment induced transient glial cell activation in several brain areas. Whether similar processes play a role in the therapeutic effect of clinically administered ECT or contribute to its side effects will require further investigations.
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6.
  • Jansson, Linda, et al. (författare)
  • Region Specific Hypothalamic Neuronal Activation and Endothelial Cell Proliferation in Response to Electroconvulsive Seizures.
  • 2006
  • Ingår i: Biological Psychiatry. - : Elsevier. - 0006-3223. ; 60:8, s. 874-881
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Major depression is often associated with disturbances in basal biological functions regulated by the hypothalamus. Electroconvulsive therapy (ECT), an efficient anti-depressant treatment. alters the activity of hypothalamic neurons. We have previously shown an increased proliferation of endothelial cells in specific areas of the rat hippocampus in response to electroconvulsive seizure (ECS) treatment, an animal model for ECT. Here we examine the effect of ECS treatment on neuronal activation and endothelial cell proliferation in mid-hypothalamus. Methods. Rats received one daily ECS treatment for 5 days and cell proliferation was detected by bromodeoxyuridine (BrdU). The number of cells double-labeled for BrdU and the endothelial cell marker rat endothelial cell antigen-1 was determined. Neuronal activation in response to acute ECS treatment was detected as c-Fos immunoreactivity in an additional experiment. Results: We demonstrate a correlating pattern of increases in neuronal activation and increased endothelial cell proliferation in the paraventricular nucleus, the supraoptic nucleus, and the ventromedial nucleus of the hypothalamus after ECS treatment. Conclusions: Hypothalamic areas with the largest increase in neuronal activation after ECS treatment exhibit increased endothelial cell proliferation. We suggest that similar angiogenic responses to ECT might counteract hypothalamic dysfunction in depressive disorder.
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8.
  • Jayatissa, Magdalena N., et al. (författare)
  • Hippocampal cytogenesis correlates to escitalopram-mediated recovery in a chronic mild stress rat model of depression
  • 2006
  • Ingår i: Neuropsychopharmacology. - : Elsevier. - 1740-634X. ; 31:11, s. 2395-2404
  • Tidskriftsartikel (refereegranskat)abstract
    • From clinical studies it is known that recurrent depressive episodes associate with a reduced hippocampal volume. Conversely, preclinical studies have shown that chronic antidepressant treatment increases hippocampal neurogenesis. Consequently, it has been suggested that a deficit in hippocampal neurogenesis is implicated in the pathophysiology of depression. To study a potential correlation between recovery and hippocampal cytogenesis, we established the chronic mild stress ( CMS) rat model of depression. When rats are subjected to CMS, several depressive symptoms develop, including the major symptom anhedonia. Rats were exposed to stress for 2 weeks and subsequently to stress in combination with antidepressant treatment for 4 consecutive weeks. The behavioral deficit measured in anhedonic animals is a reduced intake of a sucrose solution. Prior to perfusion animals were injected with bromodeoxyuridine ( BrdU), a marker of proliferating cells. Brains were sectioned horizontally and newborn cells positive for BrdU were counted in the dentate gyrus and tracked in a dorsoventral direction. CMS significantly decreased sucrose consumption and cytogenesis in the ventral part of the hippocampal formation. During exposure to the antidepressant escitalopram, given as intraperitoneally dosages of either 5 or 10 mg/kg/day, animals distributed in a bimodal fashion into a group, which recovered ( increase in sucrose consumption), and a subgroup, which refracted treatment ( no increase in sucrose consumption). Chronic treatment with escitalopram reversed the CMS-induced decrease in cytogenesis in the dentate gyrus of the ventral hippocampal formation, but in recovered animals only. Our data show a correlation between recovery from anhedonia, as measured by cessation of behavioral deficits in the CMS model, and an increase in cytogenesis in the dentate gyrus of the ventral hippocampal formation.
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9.
  • Orre, Karin, et al. (författare)
  • Chronic lithium treatment decreases NG2 cell proliferation in rat dentate hilus, amygdala and corpus callosum
  • 2009
  • Ingår i: Progress in Neuro-Psychopharmacology and Biological Psychiatry. - : Elsevier. - 0278-5846. ; 33:3, s. 503-510
  • Forskningsöversikt (refereegranskat)abstract
    • An increasing number of investigations suggest volumetric changes and glial pathology in several brain regions of patients with bipolar disorder. Lithium, used in the treatment of this disorder, has been reported to be neuroprotective and increase brain volume. Here we investigate the effect of lithium on the proliferation and survival of glial cells positive for the chondroitin sulphate proteoglycan NG2 (NG2 cells); a continuously dividing cell type implicated in remyelination and suggested to be involved in regulation of neuronal signaling and axonal outgrowth. Adult male rats were treated with lithium for four weeks and injected with the proliferation marker bromodeoxyuridine (BrdU) before or at the end of the treatment period. Immunohistochemical analysis of brain sections was performed to estimate the number of newly born (BrdU-labeled) NG2 cells and oligodendrocytes in hippocampus, basolateral nuclei of amygdala and corpus callosum. Lithium significantly decreased the proliferation of NG2 cells in dentate hilus of hippocampus, amygdala and corpus callosum, but not in the molecular layer or the cornu ammonis (CA) regions of hippocampus. The effect was more pronounced in the corpus callosum. No effect of lithium on the survival of newborn cells or the number of newly generated oligodendrocytes could be detected. Our results demonstrate that in both white and gray matter brain regions implicated in the pathophysiology of bipolar disorder, chronic lithium treatment significantly decreases the proliferation rate of NG2 cells; the major proliferating cell type of the adult brain. (C) 2009 Elsevier Inc. All rights reserved.
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