Cadmium-induced neurotoxic effects on rat basal forebrain cholinergic system through thyroid hormones disruption

Cadmium (Cd) single and repeated exposure produces cognitive dysfunctions. Basal forebrain cholinergic neu rons (BFCN) regulate cognitive functions. BFCN loss or cholinergic neurotransmission dysfunction leads to cognitive disabilities. Thyroid hormones (THs) maintain BFCN viability and functions, a...

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Detalles Bibliográficos
Autores: Sola Vendrell, Emma, Moyano-Cires Ivanoff, Paula Viviana, Flores A, García Lobo, Jimena, García Sánchez, José Manuel, Frejo Moya, María Teresa, Anadón Baselga, María José, Pelayo Alarcón, Adela, Fernández Fernández, María De La Cabeza, Del Pino J, Pino Sans, Javier Del
Tipo de recurso: artículo
Fecha de publicación:2021
País:España
Institución:Universidad Complutense de Madrid (UCM)
Repositorio:Docta Complutense
Idioma:inglés
OAI Identifier:oai:docta.ucm.es:20.500.14352/115572
Acceso en línea:https://hdl.handle.net/20.500.14352/115572
Access Level:acceso abierto
Palabra clave:615.9
Cadmium
Basal forebrain cholinergic neurons
AChE
ChAT
T3
M1R and M3R
Toxicología (Medicina)
3214 Toxicología
Descripción
Sumario:Cadmium (Cd) single and repeated exposure produces cognitive dysfunctions. Basal forebrain cholinergic neu rons (BFCN) regulate cognitive functions. BFCN loss or cholinergic neurotransmission dysfunction leads to cognitive disabilities. Thyroid hormones (THs) maintain BFCN viability and functions, and Cd disrupts their levels. However, Cd-induced BFCN damages and THs disruption involvement was not studied. To research this we treated male Wistar rats intraperitoneally with Cd once (1 mg/kg) or repetitively for 28 days (0.1 mg/kg) with/without triiodothyronine (T3, 40 µg/kg/day). Cd increased thyroid-stimulating-hormone (TSH) and decreased T3 and tetraiodothyronine (T4). Cd altered cholinergic transmission and induced a more pronounced neurodegeneration on BFCN, mediated partially by THs reduction. Additionally, Cd antagonized muscarinic 1 receptor (M1R), overexpressed acetylcholinesterase S variant (AChE-S), downregulated AChE-R, M2R, M3R and M4R, and reduced AChE and choline acetyltransferase activities through THs disruption. These results may assist to discover cadmium mechanisms that induce cognitive disabilities, revealing a new possible therapeutic tool.

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