Por favor, use este identificador para citar o enlazar este ítem: http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2600
Título : Mild Thyroid Hormone Insufficiency During Development Compromises Activity-Dependent Neuroplasticity in the Hippocampus of Adult Male Rats
Creador: ME, Gilbert
Nivel de acceso: Open access
Palabras clave : Animales
Antitiroideos - toxicidad
Conducta Animal - efectos de drogas
Conducta Animal - fisiología
Factor Neurotrófico Derivado del Encéfalo - efectos de drogas
Factor Neurotrófico Derivado del Encéfalo - genética
Factor Neurotrófico Derivado del Encéfalo - metabolismo
Condicionamiento (Psicología) - efectos de drogas
Condicionamiento (psicología) - fisiología
Hipotiroidismo Congénito - inducido químicamente
Hipotiroidismo Congénito - embriología
Hipotiroidismo Congénito - metabolismo
Femenino
Hipocampo - embriología
Hipocampo - Metabolismo
Factores de Transcripción de Tipo Kruppel - efectos de drogas
Factores de Transcripción de Tipo Kruppel - genética
Transcripción de Tipo Kruppel - metabolismo
Hombre
Factor de Crecimiento Nervioso - Efectos de drogas
Factor de Crecimiento Nervioso - genética
Factor de Crecimiento Nervioso - metabolismo
Nerve Tissue Proteins - Efectos de drogas
Nerve Tissue Proteins - genética
Nerve Tissue Proteins - metabolismo
Plasticidad Neuronal - Efectos de drogas
Plasticidad Neuronal - fisiología
Efectos Tardíos de la Exposición Prenatal - inducido químicamente
Efectos Tardíos de la Exposición Prenatal - metabolismo
Ratas
Ratas Long-Evans
Triyodotironina - deficiencia
Triyodotironina - efectos de drogas
Triyodotironina -metabolismo
Animals
Antithyroid Agents - toxicity
Behavior, Animal - drug effects
Behavior, Animal - physiology
Brain-Derived Neurotrophic Factor - drug effects
Brain-Derived Neurotrophic Factor - genetics
Brain-Derived Neurotrophic Factor - metabolism
Conditioning (Psychology) - drug effects
Conditioning (Psychology) - physiology
Congenital Hypothyroidism - chemically induced
Congenital Hypothyroidism - embryology
Congenital Hypothyroidism - metabolism
Female
Hippocampus- embryology
Hippocampus - metabolism
Kruppel-Like Transcription Factors - drug effects
Kruppel-Like Transcription Factors - genetics
Kruppel-Like Transcription Factors - metabolism
Male
Nerve Growth Factor - drug effects
Nerve Growth Factor - genetics
Nerve Growth Factor - metabolism
Nerve Tissue Proteins - drug effects
Nerve Tissue Proteins - genetics
Nerve Tissue Proteins - metabolism
Neuronal Plasticity - drug effects
Neuronal Plasticity - physiology
Pregnancy Prenatal Exposure Delayed Effects - chemically induced
Prenatal Exposure Delayed Effects - metabolism
Rats
Rats, Long-Evans
Triiodothyronine - deficiency
Triiodothyronine - drug effects
Triiodothyronine - metabolism
Agentes Antitiroideos, Hormonas Tiroideas, Neuroplasticidad, Hipocampo, Cerebro, Factor Neurotrófico Derivado del Encéfalo
Antithyroid Agents, Thyroid Hormones, Neuroplasticity, Hippocampus, Brain, Brain-Derived Neurotrophic Factor
Descripción : Severe thyroid hormone (TH) deficiency during critical phases of brain development results in irreversible neurological and cognitive impairments. The mechanisms accounting for this are likely multifactorial, and are not fully understood. Here we pursue the possibility that one important element is that TH affects basal and activity-dependent neurotrophin expression in brain regions important for neural processing. Graded exposure to propylthiouracil (PTU) during development produced dose-dependent reductions in mRNA expression of nerve growth factor (Ngf) in whole hippocampus of neonates. These changes in basal expression persisted to adulthood despite the return to euthyroid conditions in blood. In contrast to small PTU-induced reductions in basal expression of several genes, developmental PTU treatment dramatically reduced the activity-dependent expression of neurotrophins and related genes (Bdnft, Bdnfiv, Arc, and Klf9) in adulthood and was accompanied by deficits in hippocampal-based learning. These data demonstrate that mild TH insufficiency during development not only reduces expression of important neurotrophins that persists into adulthood but also severely restricts the activity-dependent induction of these genes. Considering the importance of these neurotrophins for sculpting the structural and functional synaptic architecture in the developing and the mature brain, it is likely that TH-mediated deficits in these plasticity mechanisms contribute to the cognitive deficiencies that accompany developmental TH compromise.
Colaborador(es) u otros Autores: Sanchez-Huerta K
Wood C.
Fecha de publicación : 2016
Tipo de publicación: Artículo
Formato: pdf
Identificador del Recurso : 10.1210/en.2015-1643
Fuente: Endocrinology 157(2):774-787
URI : http://repositorio.pediatria.gob.mx:8180/handle/20.500.12103/2600
Idioma: spa
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