Adulthood stress responses in rats are variably altered as a factor of adolescent stress exposure

Abstract

Stress exposure during development may influence adulthood stress response severity. The present study investigates persisting effects of two adolescent stressors upon adulthood response to predator exposure (PE). Rats were exposed to underwater trauma (UWT) or PE during adolescence, then to PE after reaching adulthood. Rats were then exposed to predator odor (PO) to test responses to predator cues alone. Behavioral and neuroendocrine assessments were conducted to determine acute effects of each stress experience. Adolescent stress altered behavioral response to adulthood PE. Acoustic startle response was blunted. Bidirectional changes in plus maze exploration were revealed as a factor of adolescent stress type. Neuroendocrine response magnitude did not predict severity of adolescent or adult stress response, suggesting that different adolescent stress events may differentially alter developmental outcomes regardless of acute behavioral or neuroendocrine response. We report that exposure to two different stressors in adolescence may differentially affect stress response outcomes in adulthood. Acute response to an adolescent stressor may not be consistent across all stressors or all dependent measures, and may not predict alterations in developmental outcomes pertaining to adulthood stress exposure. Further studies are needed to characterize factors underlying long-term effects of a developmental stressor.

Repeated elevated plus maze trials as a measure for tracking within-subjects behavioral performance in rats (Rattus norvegicus)

“…Additionally, consistent with the current results, basic movements among non-stressed control subjects were unchanged across the ten trials. This effect appears to be consistent across development as significant decreases in basic movements relative to baseline performance were also observed among adolescent rats following exposure to either predator stress or underwater trauma stress [ 8 ]. Interestingly, treatment with a nociceptin/orphanin FQ (NOP) antagonist, which has shown potential use as an anxiolytic, mitigated the behavioral effects in stressed rats without affecting this measure in the non-stressed controls [ 27 ].…”

“…The consistency of general performance measures suggests that they are robust outcome variables for detecting emotional behavioral responses to experimental manipulations over time. Our lab previously has shown that exposure to severe stress results in persistent decreases in basic movements on the EPM without changes observed in this measure among non-stressed controls [ 8 , 9 , 27 ]. Specifically, following predator stress, adult rats showed significant decreases in basic movements that were evident at 24-hours post-stress [ 9 ].…”

“…Both open arm avoidance and general performance measures on the EPM are affected by experimental manipulations, including exposure to stress or psychoactive pharmacological compounds [ 2 , 8 – 10 ]. As such, the EPM has been a useful tool for assessing pharmacological compounds for their anxiolytic potential [ 1 ], examining the impact of environmental stressors or drugs of abuse on emotional behavior [ 11 , 12 ] and investigating the neurobiological underpinnings of emotionality [ 13 ].…”

I’m Not Good for Anything and That’s Why I’m Stressed: Analysis of the Effect of Self-Efficacy and Emotional Intelligence on Student Stress Using SEM and QCA

“…Despite the importance of stress in the lives of individuals (Moore et al, 2016) and specifically in the case of university students (Lapointe et al, 2018), and the role played by EI as well as self-efficacy in the said stress, few studies have simultaneously analyzed the role played by both aspects as regard stress (Aguilar et al, 2014). In response to this, the present research aims to determine the role played by self-efficacy and EI over perceived stress.…”

Adolescent maturation of the prefrontal cortex: Role of stress and sex in shaping adult risk for compromise

“…Gonadectomy at PND28, but not PND 70, erased these sex differences in MBP expression, suggesting the necessity of circulating estrogen in the development of myelin. Although organizational influences of hormones and the influence of sex chromosomes contribute to sex differences in myelin, evidence also suggests that activational effects of hormones play at least a partial role. Studies of female to male transsexuals provide unique insight into activation effects of hormones .…”