PRIMARY OBJECTIVE: This study was designed to investigate the effect of growth hormone treatment on the proliferation of endogenous neural progenitor cells in the dentate gyrus (DG) of the brain stimulated by kainic acid (KA)-induced neurotoxicity. RESEARCH DESIGN: Neurotoxicity was induced by intraperitoneal injection of KA. GH treatment lasted 4 days, starting either immediately or after 10 days of administration of the neurotoxic insult. METHODS AND PROCEDURE: Proliferating cells were immunodetected after labelling by in vivo administration of 5-bromodeoxyuridine (BrdU). GH expression was detected by in situ hybridization and immunofluorescence. MAIN OUTCOMES AND RESULTS: KA administration stimulated the proliferation of hippocampal precursors and this effect was significantly enhanced by GH treatment. Hippocampal GH expression was also up-regulated in response to KA administration. CONCLUSIONS: The findings support the possibility that the proliferative response observed in the hippocampus of rats treated with KA and GH is a consequence of cooperation between the exogenous and the locally-produced hormone and their synergism with other mitogenic factors generated in response to the neurotoxic damage. Therefore, GH treatment could be used to cooperate with other physiological or pathological stimuli in order to promote cell proliferation.
PRIMARY OBJECTIVE: This study was designed to investigate the effect of growth hormone treatment on the proliferation of endogenous neural progenitor cells in the dentate gyrus (DG) of the brain stimulated by kainic acid (KA)-induced neurotoxicity. RESEARCH DESIGN:Neurotoxicity was induced by intraperitoneal injection of KA. GH treatment lasted 4 days, starting either immediately or after 10 days of administration of the neurotoxic insult. METHODS AND PROCEDURE: Proliferating cells were immunodetected after labelling by in vivo administration of 5-bromodeoxyuridine (BrdU). GH expression was detected by in situ hybridization and immunofluorescence. MAIN OUTCOMES AND RESULTS: KA administration stimulated the proliferation of hippocampal precursors and this effect was significantly enhanced by GH treatment. Hippocampal GH expression was also up-regulated in response to KA administration. CONCLUSIONS: The findings support the possibility that the proliferative response observed in the hippocampus of rats treated with KA and GH is a consequence of cooperation between the exogenous and the locally-produced hormone and their synergism with other mitogenic factors generated in response to the neurotoxic damage. Therefore, GH treatment could be used to cooperate with other physiological or pathological stimuli in order to promote cell proliferation.
Authors: G T Sutherland; P J Sheahan; J Matthews; C V P Dennis; D S Sheedy; T McCrossin; M A Curtis; J J Kril Journal: Exp Neurol Date: 2013-03-28 Impact factor: 5.330
Authors: Pere Barceló; Cristina Nicolau; Antoni Gamundí; Maria A Fiol; Jesús A F Tresguerres; Mourad Akaârir; Rubén V Rial Journal: Oxid Med Cell Longev Date: 2016-12-05 Impact factor: 6.543
Authors: Jesús Devesa; Alba Alonso; Natalia López; José García; Carlos I Puell; Tamara Pablos; Pablo Devesa Journal: Int J Mol Sci Date: 2017-01-23 Impact factor: 5.923
Authors: Margarita Heredia; Virginia Sánchez-Robledo; Inés Gómez; José María Criado; Antonio de la Fuente; Jesús Devesa; Pablo Devesa; Adelaida Sánchez Riolobos Journal: Int J Mol Sci Date: 2021-05-21 Impact factor: 5.923