Glucocorticoid receptor expression in blood, but not across brain regions, reveals long-term effects of early life adversity in zebra finches

Investigating the effects of acute and chronic stress on DNA damage

“…In the present experiment, chronic stress did not significantly affect dsDNA damage in erythrocytes. This was unexpected as there is evidence that erythrocytes may be particularly susceptible to dsDNA damage related to corticosterone exposure (Jimeno et al, 2023). Additionally, a previous study in our lab showed a robust increase of dsDNA damage in red blood cells with chronic stress induced by introduction to captivity (Gormally et al, 2019).…”

“…The second goal of this study was to begin to explore the mechanism of dsDNA damage with acute stress. Previous evidence suggested that both arms of the stress response should contribute to stress‐induced dsDNA damage in erythrocytes as these cells express both glucocorticoid (Jimeno et al, 2023) and beta‐adrenergic receptors (Scanes, 2015). Furthermore, both glucocorticoids and catecholamines have been shown to increase reactive oxygen species (Flaherty et al, 2017) and dsDNA damage (Flint et al, 2007) in vitro.…”

“…To assess tissue‐specific dsDNA damage with chronic stress, we quantified dsDNA damage in five tissues that play a role in the stress response (Beattie, Estrada, et al, 2022): abdominal fat and the liver as primary metabolic targets through which energy stores are mobilized (Lattin & Romero, 2013; Romero & Wingfield, 2016); the hippocampus and hypothalamus as regulators of stimulatory signals and key regulators of negative feedback (Lattin & Romero, 2015; Romero & Wingfield, 2016); and blood as the delivery system of these mediators of stress (Gormally et al, 2019; Romero & Wingfield, 2016; Sapolsky, 2000). Based on prior research, we predicted that 3 weeks of chronic stress in captivity would increase dsDNA damage in blood (Gormally et al, 2019; Malandrakis et al, 2016), but because glucocorticoid receptor expression varies in different tissues (Jimeno et al, 2023; Lattin et al, 2014), dsDNA damage in other tissues would be tissue‐specific and less predictable. We considered it likely that more metabolically active tissues, such as the liver and abdominal fat, would experience higher exposure to these stress mediators, but differences in cell turnover rates would likely play a role in the presentation of overall damage (Dollé et al, 1997; Pellettieri & Alvarado, 2007).…”