Hypothyroidism in the adult rat causes incremental changes in brain-derived neurotrophic factor, neuronal and astrocyte apoptosis, gliosis, and deterioration of postsynaptic density
Author
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Cortés, Claudia
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Eugenin, Eliseo
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Aliaga, Esteban
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Carreño, Leandro J.
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Bueno, Susan M.
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Gonzalez, Pablo A.
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Gayol, Silvina
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Naranjo, David
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Noches, Verónica
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Marassi, Michelle P.
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Rosenthal, Doris
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Jadue, Cindy
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Ibarra, Paula
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Keitel, Cecilia
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Wohllk, Nelson
Author
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Court, Fe
Admission date
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2019-03-11T13:19:36Z
Available date
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2019-03-11T13:19:36Z
Publication date
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2012
Cita de ítem
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Thyroid, Volumen 22, Issue 9, 2018, Pages 951-963
Identifier
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10507256
Identifier
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15579077
Identifier
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10.1089/thy.2010.0400
Identifier
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https://repositorio.uchile.cl/handle/2250/165675
Abstract
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Background: Adult hypothyroidism is a highly prevalent condition that impairs processes, such as learning and memory. Even though tetra-iodothyronine (T4) treatment can overcome the hypothyroidism in the majority of cases, it cannot fully recover the patient's learning capacity and memory. In this work, we analyzed the cellular and molecular changes in the adult brain occurring with the development of experimental hypothyroidism. Methods: Adult male Sprague-Dawley rats were treated with 6-propyl-2-thiouracil (PTU) for 20 days to induce hypothyroidism. Neuronal and astrocyte apoptosis were analyzed in the hippocampus of control and hypothyroid adult rats by confocal microscopy. The content of brain-derived neurotrophic factor (BDNF) was analyzed using enzyme-linked immunosorbent assay (ELISA) and in situ hybridization. The glutamatergic synapse and the postsynaptic density (PSD) were analyzed by electron microscopy. The content of PSD proteins like tyrosine receptor kinase B (TrkB), p75
Hypothyroidism in the adult rat causes incremental changes in brain-derived neurotrophic factor, neuronal and astrocyte apoptosis, gliosis, and deterioration of postsynaptic density