Early life stress and psychopharmacology

Abstract

The concept of early life stress (ELS) has long been a central focus in clinical psychiatry and psychology, owing in no small part to the primacy of this concept in psychoanalytic theory. Perhaps in response to that legacy, both clinical and preclinical biologically oriented researchers have become increasingly invested in understanding the adult sequelae of adverse environmental factors occurring early in development.Several factors stand out in considering the drivers of this changing zeitgeist: (1) new efforts to integrate preclinical and clinical findings on the pathogenesis of major psychiatric disorders, especially by focusing on model neurobiological systems (e.g., Heim et al. 1997); (2) empirical demonstration of the relevance of the classic diathesis-stress theory using gene×environment (G×E) experimental designs (e.g., Caspi et al. 2003) and, more recently, epigenetic approaches (e.g., McGowan and Szyf 2010); (3) increased recognition of the adverse psychiatric and biomedical sequelae of ELS (e.g., Gluckman and Hanson 2004;Scott et al. 2010); (4) convincing demonstration of ELS as a major global public health challenge (e.g., Krug et al. 2002). The diversity of work covered in this Special Issue reflects the remarkable progress that has been made in this area in a relatively brief span of time. Long-term cognitive sequelae of ELS are now well documented, and two reviews in this issue address this burgeoning literature. Hedges and Woon (2010) organize the findings with an emphasis on specific functional effects, while Pechtel and Pizzagali (2010) utilize a neurodevelopmental framework to integrate observations on cognitive and affective processes.The seminal preclinical studies of ELS and the HPA axis (Claessens et al.

Spatial Learning Is Impaired in Male Pubertal Rats Following Neonatal Daily but Not Randomly Spaced Maternal Deprivation

“…For the intermittent/pseudo-randomly spaced MD model, separation is not daily and does not occur at regular intervals (van Oers, 1998;Lehmann et al, 1999;Weaver et al, 2007). In this model, reductions in basal CORT (Kuhn and Schanberg, 1998;Daskalakis et al, 2011), increased sensitivity to glucocorticoid negative feedback (Kuhn and Schanberg, 1998;De Kloet et al, 2005;Daskalakis et al, 2011), increased adaptability to social settings (De Kloet et al, 2005;Oomen et al, 2010), and improved emotional resilience are evident (Price and Steckler, 2011;Schmidt et al, 2011). Because these different separation schedules have been employed independently, contrasting reports could result from any number of undocumented variables.…”