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Pharmacol Res. 2016 Jul;109:64-73. doi: 10.1016/j.phrs.2015.12.033. Epub 2016 Jan 14.

Long-term effects of early life stress exposure: Role of epigenetic mechanisms.

Author information

1
Centro de Estudios Farmacológicos y Botánicos (CEFYBO-CONICET), 1ª Cátedra de Farmacología, Facultad de Medicina, UBA, Paraguay 2155, Piso 15, C1121ABG Ciudad Autónoma de Buenos Aires, Argentina.
2
Instituto de Investigaciones Farmacológicas (ININFA), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires (UBA), Junín 956, 5(to) piso, C1113AAD, Ciudad Autónoma de Buenos Aires, Argentina. Electronic address: gacosta@ffyb.uba.ar.

Abstract

Stress is an adaptive response to demands of the environment and thus essential for survival. Exposure to stress during the first years of life has been shown to have profound effects on the growth and development of an adult individual. There are evidences demonstrating that stressful experiences during gestation or in early life can lead to enhanced susceptibility to mental disorders. Early-life stress triggers hypothalamic-pituitary-adrenocortical (HPA) axis activation and the associated neurochemical reactions following glucocorticoid release are accompanied by a rapid physiological response. An excessive response may affect the developing brain resulting in neurobehavioral and neurochemical changes later in life. This article reviews the data from experimental studies aimed to investigate hormonal, functional, molecular and epigenetic mechanisms involved in the stress response during early-life programming. We think these studies might prove useful for the identification of novel pharmacological targets for more effective treatments of mental disorders.

KEYWORDS:

BDNF; HDAC inhibitors; HPA axis; Maternal separation; Prenatal stress; Sodium butyrate; Stress response; Suberanilohydroxamic acid (SAHA); Trichostatin A (TSA); Valproic acid

PMID:
26774789
DOI:
10.1016/j.phrs.2015.12.033
[Indexed for MEDLINE]

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