Dehydroepiandrosterone increases the number and dendrite maturation of doublecortin cells in the dentate gyrus of middle age male Wistar rats exposed to chronic mild stress


Por: Herrera-Perez, J. J., Martinez-Mota, L., Jimenez-Rubio, G., Ortiz-Lopez, L., Cabrera-Munoz, E. A., Galindo-Sevilla, N., Zambrano, E., Hernandez-Luis, F., Ramirez-Rodriguez, G. B., Flores-Ramos, M.

Publicada: 15 mar 2017
Categoría: Behavioral neuroscience

Resumen:
Aging increases the vulnerability to stress and risk of developing depression. These changes have been related to a reduction of dehydroepiandrosterone (DHEA) levels, an adrenal steroid with anti stress effects. Also, adult hippocampal neurogenesis decreases during aging and its alteration or impaired is related to the development of depression. Besides, it has been hypothesized that DHEA increases the formation of new neurons. However, it is unknown whether treatment with DHEA in aging may stimulate the dendrite maturation of newborn neurons and reversing depressive-like signs evoked by chronic stress exposure. Here aged male rats (14 months old) were subjected to a scheme of chronic mild stress (CMS) during six weeks, received a treatment with DHEA from the third week of CMS. Changes in body weight and sucrose preference (SP) were measured once a week. DHEA levels were measured in serum, identification of doublecortin-(DCX)-, BrdU- and BrdU/NeuN-labeled cells was done in the dentate gyrus of the hippocampus. CMS produced a gradual reduction in the body weight, but no changes in the SP were observed. Treatment enhanced levels of DHEA, but lack of recovery on body weight of stressed rats. Aging reduced the number of DCX-, BrdU- and BrdU/NeuN-cells but DHEA just significantly increased the number of DCX-cells in rats under CMS and controls, reaching levels of young non-stressed rats (used here as a reference of an optimal status of health). In rats under CMS, DHEA facilitated dendritic maturation of immature new neurons. Our results reveal that DHEA improves neural plasticity even in conditions of CMS in middle age rats. Thus, this hormone reverted the decrement of DCX-cells caused during normal aging. (C) 2017 Elsevier B.V. All rights reserved.

Filiaciones:
Herrera-Perez, J. J.:
 Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Direcc Invest Neurociencias, Farmacol Conductual, Calzada Mexico Xochimilco 101, Mexico City 14370, DF, Mexico

Martinez-Mota, L.:
 Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Direcc Invest Neurociencias, Farmacol Conductual, Calzada Mexico Xochimilco 101, Mexico City 14370, DF, Mexico

Jimenez-Rubio, G.:
 Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Direcc Invest Neurociencias, Farmacol Conductual, Calzada Mexico Xochimilco 101, Mexico City 14370, DF, Mexico

Ortiz-Lopez, L.:
 Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Subdirecc Invest Clin, Lab Neurogenesis, Calzada Mexico Xochimilco 101, Mexico City 14370, DF, Mexico

Cabrera-Munoz, E. A.:
 Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Subdirecc Invest Clin, Lab Neurogenesis, Calzada Mexico Xochimilco 101, Mexico City 14370, DF, Mexico

Galindo-Sevilla, N.:
 Inst Nacl Perinatol, Dept Infectol & Inmunol, Montes Urales 800, Mexico City 11000, DF, Mexico

Zambrano, E.:
 Inst Nacl Ciencias Med & Nutr Salvador Zubiran, Dept Anim Nutr, Ave Vasco de Quiroga 15, Mexico City 14080, DF, Mexico

Hernandez-Luis, F.:
 Univ Nacl Autonoma Mexico, Fac Quim, Dept Farm, Circuito Exterior S-N, Mexico City 04510, DF, Mexico

Ramirez-Rodriguez, G. B.:
 Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Subdirecc Invest Clin, Lab Neurogenesis, Calzada Mexico Xochimilco 101, Mexico City 14370, DF, Mexico

Flores-Ramos, M.:
 Catedrat Consejo Nacl Ciencia & Tecnol, Ave Insurgentes Sur 1582, Mexico City 03940, DF, Mexico

 Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Clin Trastornos Afect, Calzada Mexico Xochimilco 101, Mexico City 14370, DF, Mexico
ISSN: 01664328
Editorial
ELSEVIER SCIENCE BV, PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS, Países Bajos
Tipo de documento: Article
Volumen: 321 Número:
Páginas: 137-147
WOS Id: 000394403600016
ID de PubMed: 28062256

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