Neuronal plasticity and antidepressants in the diabetic brain
The hippocampus, a limbic structure linked to higher brain functions, appears vulnerable in diabetic subjects that have a higher risk of stroke, dementia, and cognitive decline. The dentate gyrus (DG) of the hippocampus is one of the limited neurogenic brain areas during adulthood; neurons born in t...
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2009
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00778923_v1153_n_p203_Beauquis http://hdl.handle.net/20.500.12110/paper_00778923_v1153_n_p203_Beauquis |
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paper:paper_00778923_v1153_n_p203_Beauquis2023-06-08T15:07:30Z Neuronal plasticity and antidepressants in the diabetic brain Dentate gyrus Fluoxetine Hippocampus Neurogenesis Type 1 diabetes antidepressant agent fluoxetine animal cell animal experiment animal model animal tissue brain damage brain disease cell density cell differentiation cell proliferation conference paper controlled study corticosterone blood level dentate gyrus diabetes mellitus drug effect hippocampus insulin dependent diabetes mellitus limbic cortex mouse nerve cell nerve cell plasticity nonhuman phenotype streptozocin diabetes stress Animalia Mus The hippocampus, a limbic structure linked to higher brain functions, appears vulnerable in diabetic subjects that have a higher risk of stroke, dementia, and cognitive decline. The dentate gyrus (DG) of the hippocampus is one of the limited neurogenic brain areas during adulthood; neurons born in the DG are involved in some types of learning and memory processes. We found a decrease in the ability for proliferation and neuronal differentiation of newborn cells, measured by bromodeoxyuridine incorporation in the DG, from streptozotocin-induced diabetic mice. The hilar region, formed by mature neurons presenting higher sensitivity to brain damage, showed a reduced neuronal density in diabetic mice with respect to vehicle-treated mice. Interestingly, in a spontaneous model of type 1 diabetes, we corroborated a decrease in the rate of neurogenesis in the nonobese diabetic mice compared to control strains, and this reduction was also found during the prediabetic stage. The antidepressant fluoxetine administered over a period of 10 days to diabetic mice was effective in preventing changes in proliferation and differentiation of new neurons. Confocal microscope studies, including using neuronal and glial markers, suggested that differentiation toward a neuronal phenotype was decreased in diabetic animals and was reversed by the antidepressant treatment. In addition, the loss of hilar neurons was avoided by fluoxetine treatment. Several reports have demonstrated that high susceptibility to stress and elevated corticosterone levels are detrimental to neurogenesis and contribute to neuronal loss. These features are common in some types of depression, diabetes, and aging processes, suggesting they participate in the reported hippocampal abnormalities present in these conditions. © 2009 New York Academy of Sciences. 2009 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00778923_v1153_n_p203_Beauquis http://hdl.handle.net/20.500.12110/paper_00778923_v1153_n_p203_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 |
Dentate gyrus Fluoxetine Hippocampus Neurogenesis Type 1 diabetes antidepressant agent fluoxetine animal cell animal experiment animal model animal tissue brain damage brain disease cell density cell differentiation cell proliferation conference paper controlled study corticosterone blood level dentate gyrus diabetes mellitus drug effect hippocampus insulin dependent diabetes mellitus limbic cortex mouse nerve cell nerve cell plasticity nonhuman phenotype streptozocin diabetes stress Animalia Mus |
| spellingShingle |
Dentate gyrus Fluoxetine Hippocampus Neurogenesis Type 1 diabetes antidepressant agent fluoxetine animal cell animal experiment animal model animal tissue brain damage brain disease cell density cell differentiation cell proliferation conference paper controlled study corticosterone blood level dentate gyrus diabetes mellitus drug effect hippocampus insulin dependent diabetes mellitus limbic cortex mouse nerve cell nerve cell plasticity nonhuman phenotype streptozocin diabetes stress Animalia Mus Neuronal plasticity and antidepressants in the diabetic brain |
| topic_facet |
Dentate gyrus Fluoxetine Hippocampus Neurogenesis Type 1 diabetes antidepressant agent fluoxetine animal cell animal experiment animal model animal tissue brain damage brain disease cell density cell differentiation cell proliferation conference paper controlled study corticosterone blood level dentate gyrus diabetes mellitus drug effect hippocampus insulin dependent diabetes mellitus limbic cortex mouse nerve cell nerve cell plasticity nonhuman phenotype streptozocin diabetes stress Animalia Mus |
| description |
The hippocampus, a limbic structure linked to higher brain functions, appears vulnerable in diabetic subjects that have a higher risk of stroke, dementia, and cognitive decline. The dentate gyrus (DG) of the hippocampus is one of the limited neurogenic brain areas during adulthood; neurons born in the DG are involved in some types of learning and memory processes. We found a decrease in the ability for proliferation and neuronal differentiation of newborn cells, measured by bromodeoxyuridine incorporation in the DG, from streptozotocin-induced diabetic mice. The hilar region, formed by mature neurons presenting higher sensitivity to brain damage, showed a reduced neuronal density in diabetic mice with respect to vehicle-treated mice. Interestingly, in a spontaneous model of type 1 diabetes, we corroborated a decrease in the rate of neurogenesis in the nonobese diabetic mice compared to control strains, and this reduction was also found during the prediabetic stage. The antidepressant fluoxetine administered over a period of 10 days to diabetic mice was effective in preventing changes in proliferation and differentiation of new neurons. Confocal microscope studies, including using neuronal and glial markers, suggested that differentiation toward a neuronal phenotype was decreased in diabetic animals and was reversed by the antidepressant treatment. In addition, the loss of hilar neurons was avoided by fluoxetine treatment. Several reports have demonstrated that high susceptibility to stress and elevated corticosterone levels are detrimental to neurogenesis and contribute to neuronal loss. These features are common in some types of depression, diabetes, and aging processes, suggesting they participate in the reported hippocampal abnormalities present in these conditions. © 2009 New York Academy of Sciences. |
| title |
Neuronal plasticity and antidepressants in the diabetic brain |
| title_short |
Neuronal plasticity and antidepressants in the diabetic brain |
| title_full |
Neuronal plasticity and antidepressants in the diabetic brain |
| title_fullStr |
Neuronal plasticity and antidepressants in the diabetic brain |
| title_full_unstemmed |
Neuronal plasticity and antidepressants in the diabetic brain |
| title_sort |
neuronal plasticity and antidepressants in the diabetic brain |
| publishDate |
2009 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00778923_v1153_n_p203_Beauquis http://hdl.handle.net/20.500.12110/paper_00778923_v1153_n_p203_Beauquis |
| _version_ |
1768543460839653376 |