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Sökning: WFRF:(Tingström Anders)

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  • Föregående 12[3]45Nästa
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21.
  • 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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22.
  • 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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24.
  • Jansson, Linda, et al. (författare)
  • Repeated electroconvulsive seizures increase the number of vessel-associated macrophages in rat hippocampus.
  • 2012
  • Ingår i: Journal of ECT. - : Lippincott Williams & Wilkins. - 1533-4112. ; 28:3, s. 174-179
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVES: We have previously reported that electroconvulsive seizure (ECS)-an animal model of the antidepressant treatment electroconvulsive therapy-causes glial cell activation in hippocampus and other limbic areas. In the current study, we have investigated whether the cellular response to ECS includes recruitment and infiltration of nonresident macrophages into the hippocampal brain parenchyma. METHODS: Adult rats received 1 ECS daily for 10 consecutive days and were then killed at different time points after the last ECS treatment. Brain sections were immunostained for laminin, a matrix protein expressed in the basal membrane of blood vessels, in combination with anti-CD163, which identifies mature blood-borne macrophages. The number of CD163 cells in the hippocampus was quantified. We also investigated the number of vessel-associated cells expressing CD4 and major histocompatibility complex class II (MHC II). CD4 is mainly expressed by CD4 T cells, but can also be found on macrophages, monocytes, and activated microglia, whereas MHC II is expressed by macrophages, activated microglia, dendritic cells, and B cells. RESULTS: Our results demonstrate increased numbers of CD163 and CD4 cells following ECS. Most CD4 cells within the vasculature had a similar morphology to the CD163 macrophages. No CD163 cells were detected outside the vessels but a subpopulation of CD4 cells was seen in the brain parenchyma, here with a morphology resembling microglia. There was a transient increase in the number of blood vessel-associated MHC II cells following ECS. CONCLUSIONS: Our observations showed that the cellular response to ECS involves recruitment of blood-derived macrophages, but we could not see any infiltration into the brain parenchyma of these cells.
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25.
  • 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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28.
  • Madsen, T M, et al. (författare)
  • Increased neurogenesis in a model of electroconvulsive therapy
  • 2000
  • Ingår i: Biological Psychiatry. - : Elsevier. - 0006-3223. ; 47:12, s. 1043-1049
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Electroconvulsive therapy (ECT) is a widely used and efficient treatment modality in psychiatry, although the basis for its therapeutic effect is still unknown. Past research has shown seizure activity to be a regulator of neurogenesis in the adult brain. This study examines the effect of a single and multiple electroconvulsive seizures on neurogenesis in the rat dentate gyrus. METHODS: Rats were given either a single or a series of 10 electroconvulsive seizures. At different times after the seizures, a marker of proliferating cells, Bromodeoxyuridine (BrdU), was administered to the animals. Subsequently, newborn cells positive for BrdU were counted in the dentate gyrus. Double staining with a neuron-specific marker indicated that the newborn cells displayed a neuronal phenotype. RESULTS: A single electroconvulsive seizure significantly increased the number of new born cells in the dentate gyrus. These cells survived for at least 3 months. A series of seizures further increased neurogenesis, indicating a dose-dependent mechanism. CONCLUSIONS: We propose that generation of new neurons in the hippocampus may be an important neurobiologic element underlying the clinical effects of electroconvulsive seizures.
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29.
  • Nordgren, Max, et al. (författare)
  • Orchestrated Regulation of Nogo Receptors, Lotus, AMPA Receptors and BDNF in an ECT Model Suggests Opening and Closure of a Window of Synaptic Plasticity
  • 2013
  • Ingår i: PLoS ONE. - : Public Library of Science. - 1932-6203. ; 8:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Electroconvulsive therapy (ECT) is an efficient and relatively fast acting treatment for depression. However, one severe side effect of the treatment is retrograde amnesia, which in certain cases can be long-term. The mechanisms behind the antidepressant effect and the amnesia are not well understood. We hypothesized that ECT causes transient downregulation of key molecules needed to stabilize synaptic structure and to prevent Ca2+ influx, and a simultaneous increase in neurotrophic factors, thus providing a short time window of increased structural synaptic plasticity. Here we followed regulation of NgR1, NgR3, LOTUS, BDNF, and AMPA subunits GluR1 and GluR2 flip and flop mRNA levels in hippocampus at 2, 4, 12, 24, and 72 hours after a single episode of induced electroconvulsive seizures (ECS) in rats. NgR1 and LOTUS mRNA levels were transiently downregulated in the dentate gyrus 2, 4, 12 and 4, 12, 24 h after ECS treatment, respectively. GluR2 flip, flop and GluR1 flop were downregulated at 4 h. GluR2 flip remained downregulated at 12 h. In contrast, BDNF, NgR3 and GluR1 flip mRNA levels were upregulated. Thus, ECS treatment induces a transient regulation of factors important for neuronal plasticity. Our data provide correlations between ECS treatment and molecular events compatible with the hypothesis that both effects and side effects of ECT may be caused by structural synaptic rearrangements.
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