Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: Reversion by antidepressant treatment
Cerebral dysfunctions, including a high incidence of depression, are common findings in human type 1 diabetes mellitus. An association between depression and defective hippocampal neurogenesis has been proposed and, in rodents, antidepressant therapy restores neuronal proliferation in the dentate gy...
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2006
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paper:paper_0953816X_v23_n6_p1539_Beauquis2023-06-08T15:55:28Z Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: Reversion by antidepressant treatment 5-bromo-2′-deoxyuridine Dentate gyrus Fluoxetine Type 1 diabetes antidepressant agent beta tubulin beta tubulin iii broxuridine cell marker fluoxetine glial fibrillary acidic protein serotonin uptake inhibitor unclassified drug animal experiment animal model animal tissue article astrocyte brain dysfunction cell proliferation confocal microscopy controlled study dentate gyrus depression disease association drug effect hippocampus insulin dependent diabetes mellitus male mouse nerve cell plasticity nervous system development neuroblast nonhuman phenotype priority journal streptozocin diabetes Animals Antidepressive Agents, Second-Generation Bromodeoxyuridine Cell Count Cell Proliferation Cytoplasmic Granules Diabetes Mellitus, Experimental Fluorescent Antibody Technique Fluoxetine Hippocampus Immunohistochemistry Male Mice Mice, Inbred C57BL Microscopy, Confocal Neuroglia Neuronal Plasticity Neurons Cerebral dysfunctions, including a high incidence of depression, are common findings in human type 1 diabetes mellitus. An association between depression and defective hippocampal neurogenesis has been proposed and, in rodents, antidepressant therapy restores neuronal proliferation in the dentate gyrus. Hippocampal neurogenesis is also deficient in diabetic mice, which led us to study whether the selective serotonin reuptake inhibitor fluoxetine influences cell proliferation in streptozotocin-diabetic animals. Diabetic and control C57BL/6 mice received fluoxetine (10 mg/kg/day, i.p., 10 days) and dentate gyrus cell proliferation was measured after a single injection of 5-bromo-2′-deoxyuridine (BrdU). Diabetic mice showed reduced cell proliferation. Fluoxetine treatment, although having no effect in controls, corrected this parameter in diabetic mice. The phenotype of newly generated cells was analysed by confocal microscopy after seven daily BrdU injections, using Tuj-1/β-III tubulin as a marker for immature neurones and glial fibrillary acidic protein for astrocytes. In controls, the proportion of Tuj-1-BrdU-positive cells over total BrdU cells was ∼70%. In vehicle-treated diabetic mice, immature neurones decreased to 56% and fluoxetine brought this proportion back to control values without affecting astrocytes. Therefore, fluoxetine preferentially increased the proliferation of cells with a neuronal phenotype. In addition, neurones were counted in the hilus of the dentate gyrus; a 30% decrease was found in diabetic mice compared with controls, whereas this neuronal loss was prevented by fluoxetine. In conclusion, fluoxetine treatment restored neuroplasticity-related hippocampal alterations of diabetic mice. These findings may be potentially important to counteract diabetes-associated depression in humans. © The Authors (2006). 2006 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0953816X_v23_n6_p1539_Beauquis http://hdl.handle.net/20.500.12110/paper_0953816X_v23_n6_p1539_Beauquis |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
5-bromo-2′-deoxyuridine Dentate gyrus Fluoxetine Type 1 diabetes antidepressant agent beta tubulin beta tubulin iii broxuridine cell marker fluoxetine glial fibrillary acidic protein serotonin uptake inhibitor unclassified drug animal experiment animal model animal tissue article astrocyte brain dysfunction cell proliferation confocal microscopy controlled study dentate gyrus depression disease association drug effect hippocampus insulin dependent diabetes mellitus male mouse nerve cell plasticity nervous system development neuroblast nonhuman phenotype priority journal streptozocin diabetes Animals Antidepressive Agents, Second-Generation Bromodeoxyuridine Cell Count Cell Proliferation Cytoplasmic Granules Diabetes Mellitus, Experimental Fluorescent Antibody Technique Fluoxetine Hippocampus Immunohistochemistry Male Mice Mice, Inbred C57BL Microscopy, Confocal Neuroglia Neuronal Plasticity Neurons |
| spellingShingle |
5-bromo-2′-deoxyuridine Dentate gyrus Fluoxetine Type 1 diabetes antidepressant agent beta tubulin beta tubulin iii broxuridine cell marker fluoxetine glial fibrillary acidic protein serotonin uptake inhibitor unclassified drug animal experiment animal model animal tissue article astrocyte brain dysfunction cell proliferation confocal microscopy controlled study dentate gyrus depression disease association drug effect hippocampus insulin dependent diabetes mellitus male mouse nerve cell plasticity nervous system development neuroblast nonhuman phenotype priority journal streptozocin diabetes Animals Antidepressive Agents, Second-Generation Bromodeoxyuridine Cell Count Cell Proliferation Cytoplasmic Granules Diabetes Mellitus, Experimental Fluorescent Antibody Technique Fluoxetine Hippocampus Immunohistochemistry Male Mice Mice, Inbred C57BL Microscopy, Confocal Neuroglia Neuronal Plasticity Neurons Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: Reversion by antidepressant treatment |
| topic_facet |
5-bromo-2′-deoxyuridine Dentate gyrus Fluoxetine Type 1 diabetes antidepressant agent beta tubulin beta tubulin iii broxuridine cell marker fluoxetine glial fibrillary acidic protein serotonin uptake inhibitor unclassified drug animal experiment animal model animal tissue article astrocyte brain dysfunction cell proliferation confocal microscopy controlled study dentate gyrus depression disease association drug effect hippocampus insulin dependent diabetes mellitus male mouse nerve cell plasticity nervous system development neuroblast nonhuman phenotype priority journal streptozocin diabetes Animals Antidepressive Agents, Second-Generation Bromodeoxyuridine Cell Count Cell Proliferation Cytoplasmic Granules Diabetes Mellitus, Experimental Fluorescent Antibody Technique Fluoxetine Hippocampus Immunohistochemistry Male Mice Mice, Inbred C57BL Microscopy, Confocal Neuroglia Neuronal Plasticity Neurons |
| description |
Cerebral dysfunctions, including a high incidence of depression, are common findings in human type 1 diabetes mellitus. An association between depression and defective hippocampal neurogenesis has been proposed and, in rodents, antidepressant therapy restores neuronal proliferation in the dentate gyrus. Hippocampal neurogenesis is also deficient in diabetic mice, which led us to study whether the selective serotonin reuptake inhibitor fluoxetine influences cell proliferation in streptozotocin-diabetic animals. Diabetic and control C57BL/6 mice received fluoxetine (10 mg/kg/day, i.p., 10 days) and dentate gyrus cell proliferation was measured after a single injection of 5-bromo-2′-deoxyuridine (BrdU). Diabetic mice showed reduced cell proliferation. Fluoxetine treatment, although having no effect in controls, corrected this parameter in diabetic mice. The phenotype of newly generated cells was analysed by confocal microscopy after seven daily BrdU injections, using Tuj-1/β-III tubulin as a marker for immature neurones and glial fibrillary acidic protein for astrocytes. In controls, the proportion of Tuj-1-BrdU-positive cells over total BrdU cells was ∼70%. In vehicle-treated diabetic mice, immature neurones decreased to 56% and fluoxetine brought this proportion back to control values without affecting astrocytes. Therefore, fluoxetine preferentially increased the proliferation of cells with a neuronal phenotype. In addition, neurones were counted in the hilus of the dentate gyrus; a 30% decrease was found in diabetic mice compared with controls, whereas this neuronal loss was prevented by fluoxetine. In conclusion, fluoxetine treatment restored neuroplasticity-related hippocampal alterations of diabetic mice. These findings may be potentially important to counteract diabetes-associated depression in humans. © The Authors (2006). |
| title |
Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: Reversion by antidepressant treatment |
| title_short |
Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: Reversion by antidepressant treatment |
| title_full |
Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: Reversion by antidepressant treatment |
| title_fullStr |
Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: Reversion by antidepressant treatment |
| title_full_unstemmed |
Reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: Reversion by antidepressant treatment |
| title_sort |
reduced hippocampal neurogenesis and number of hilar neurones in streptozotocin-induced diabetic mice: reversion by antidepressant treatment |
| publishDate |
2006 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0953816X_v23_n6_p1539_Beauquis http://hdl.handle.net/20.500.12110/paper_0953816X_v23_n6_p1539_Beauquis |
| _version_ |
1768543332841029632 |