Active behavioral coping alters the behavioral but not the endocrine response to stress

Abstract

Summary Exposure to traumatic stressors typically causes lasting changes in emotionality and behavior. However, coping strategies have been shown to prevent and alleviate many stress consequences and the biological mechanisms that underlie coping are of great interest. Whereas the laboratory stressor inescapable tail-shock induces anxiety-like behaviors, here we demonstrate that permitting a rat to chew on a wooden dowel during administration of tail-shock prevented the development of anxiety like behaviors in the open field and juvenile social exploration tests. Uncontrollable stressors increase corticosterone and decrease thyroid hormone, and we hypothesized that coping would blunt these changes. While tail-shock did produce these effects, active coping did not alter hormone levels. The dissociation between behavioral resilience and circulating hormones is discussed with regard to the utility of these molecules as biomarkers for psychiatric disease.

Behavioral Traits Associated With Resilience to the Effects of Repeated Social Defeat on Cocaine-Induced Conditioned Place Preference in Mice

“…Future works should address ways to increase resilience in vulnerable animals. The negative consequences of stress can be reduced through environmental manipulations (Greenwood and Fleshner, 2008;Schloesser et al, 2010;MacKay et al, 2017) and by allowing mastication during stress exposure, a model of active behavioral coping in rodents (Hennessy and Foy, 1987;Hori et al, 2004;Kubo et al, 2009;Stalnaker et al, 2009;Helmreich et al, 2012). Finally, it is important to study the neurobiological substrates of resilience, which underly the behavioral phenotypes observed in our study.…”

Chronic Suppression of Glucagon-Like Peptide-1 Receptor (GLP1R) mRNA Translation in the Rat Bed Nucleus of the Stria Terminalis Reduces Anxiety-Like Behavior and Stress-Induced Hypophagia, But Prolongs Stress-Induced Elevation of Plasma Corticosterone

“…Although baseline (i.e., prestress) cort levels did not differ between GLP1R-KD and CTRL rats, it is possible that GLP1R-KD rats in our study had more pronounced cort responses to behavioral testing and day-to-day disruptions (e.g., body weight assessments), such that they experienced more total exposure to circulating cort than CTRL rats, despite their generally "less anxious" phenotype. Published studies focused on projection pathways arising from the alBST (Johnson et al, 2016) and on GLP1R signaling in other stress-related circuits that also have documented dissociations between behavioral and endocrine responses to acute stress, including differential effects of manipulating GLP1R signaling within different forebrain regions (Kinzig et al, 2003;Helmreich et al, 2012;Ghosal et al, 2017). Such studies support the dissociability of central neural circuits controlling physiological and behavioral responses to stress-inducing stimuli and treatments.…”

Learned helplessness at fifty: Insights from neuroscience.

“…But, at least in the rodent, it does not (see Dess, Linwick, Patterson, Overmier, & Levine, 1983 for different results in dogs). In the rodent, the corticosterone rise is not greater or more prolonged (Helmreich et al, 2012; Maier et al, 1986), the adrenocorticotrophic hormone rise is not greater or more prolonged (Maier et al, 1986), nor is the increase in corticotropin releasing hormone in the hypothalamus larger (Helmreich et al, 1999). This unexpected finding has been inexplicable by psychological theory or behavioral considerations.…”