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Prolactin reduces the kainic acid-induced increase in intracellular Ca2+ concentration, leading to neuroprotection of hippocampal neurons.
Rodríguez-Chávez, V; Flores-Soto, E; Molina-Salinas, G; Martínez-Razo, L D; Montaño, L M; Cerbón, M.
Afiliación
  • Rodríguez-Chávez V; Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México (UNAM), CDMX 04510, Mexico.
  • Flores-Soto E; Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), CDMX 04360, Mexico.
  • Molina-Salinas G; Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México (UNAM), CDMX 04510, Mexico.
  • Martínez-Razo LD; Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México (UNAM), CDMX 04510, Mexico.
  • Montaño LM; Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), CDMX 04360, Mexico.
  • Cerbón M; Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de México (UNAM), CDMX 04510, Mexico. Electronic address: marcocerbon@quimica.unam.mx.
Neurosci Lett ; 810: 137344, 2023 07 27.
Article en En | MEDLINE | ID: mdl-37315731
The aim of this study was to determine the effect of prolactin (PRL) on intracellular calcium (Ca2+) concentration and its neuroprotective role in a model of kainic acid (KA) excitotoxicity in primary cultures of hippocampal neurons. Cell viability and intracellular Ca2+ concentrations were determined by MTT and Fura-2 assays, respectively, either after induction by KA as an agonist or after treatment with NBQX antagonist alone or in combination with PRL administration. Expression of ionotropic glutamatergic receptors (iGluRs) subunits in neuronal cells was determined by RT-qPCR. Dose-response treatments with KA or glutamate (Glu), the latter used as endogenous agonist control, induced a significant increase in neuronal intracellular Ca2+ concentration followed by a significant decrease in hippocampal neuronal viability. Administration of PRL induced a significant increase in neuronal viability after treatment with KA. Furthermore, administration of PRL decreased intracellular Ca2+ concentrations induced by KA treatment. Independent administration of the AMPAR-KAR antagonist reversed cell death and reduced intracellular Ca2+ concentration in a similar manner as PRL. Additionally, mRNA expression of AMPAR, KAR and NMDAR subtypes were detected in hippocampal neurons; however, no significant changes in iGluRs subunit expression were observed due to excitotoxicity or PRL treatment. The results suggest that PRL inhibits the increase in intracellular Ca2+ concentration induced by KA, leading to neuroprotection.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Prolactina / Ácido Kaínico Idioma: En Revista: Neurosci Lett Año: 2023 Tipo del documento: Article País de afiliación: México Pais de publicación: Irlanda

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Prolactina / Ácido Kaínico Idioma: En Revista: Neurosci Lett Año: 2023 Tipo del documento: Article País de afiliación: México Pais de publicación: Irlanda