Abstract
Coping strategies, the first line of defense against adversities, develop through experience. There is consistent evidence that both genotype and sex contribute to the development of dysfunctional coping, leading to maladaptive outcomes of adverse experiences or to adaptive coping that fosters rapid recovery even from severe stress. However, how these factors interact to influence the development of individual coping strategies is just starting to be investigated. In the following review, we will consider evidence that experience, sex, and genotype influence the brain circuits and neurobiological processes involved in coping with adversities and discuss recent results pointing to the specific effects of the interaction between early experiences, genotype, and stress in the development of functional and dysfunctional coping styles.
Highlights
Stress is the main non-genetic source of psychopathology
Depletion of medial pre-frontal cortex (mpFC) DA by local infusion of 6-hydroxydopamine (6OHDA) prevents Forced Swimming Test (FST)-induced inhibition of mesoaccumbens DA as well as induction of immobility in B6 male mice and a chronic antidepressant treatment moderates FST-induced enhancement of mpFC DA, inhibition of mesoaccumbens DA as well as immobility in male mice of this strain (Ventura et al, 2004). These findings offer strong support to the hypothesis that genotype-dependent variations of mpFC DA response to stress moderate the development of passive coping strategies in inescapable/unavoidable stressful conditions
Evidence collected by Maier and coworkers indicate that: (1) a corticostriatal circuit connecting medial pre-frontal Cortex (mPFC) to posterior dorsomedial striatum (DMS) is involved in the appraisal of a stressful experience as controllable/escapable; (2) appraisal of Escapable Stress (ES) inhibits dorsal raphe nucleus (DRN) 5-HT neurons through excitatory inputs from the mpFC to intrinsic GABAergic neurons, leading to a rapid reduction of 5-HT release induced by the shock experience (Maier and Seligman, 2016); and (3) the learned helplessness syndrome is due to desensitization of DRN 5-HT1A inhibitory auto-receptors (Maier, 2015)
Summary
Stress is the main non-genetic source of psychopathology. the identification of mechanisms capable of moderating the pathogenic effects of stress is a major goal of clinical and preclinical research. Coping Styles, Sex and Genotype hormone, and corticosterone/cortisol (Vermetten and Bremner, 2002; Bonne et al, 2004; McEwen and Gianaros, 2011) Both emotional and physiological responses are shared with non-human animals and support the organism’s ability to sustain the challenging experiences. Certain coping styles, such as proactive coping, are associated with low flexibility and impulsivity in mice (Coppens et al, 2010) These considerations foster the hypothesis that individual coping styles are the results of the interaction between genotype, stress experiences, and sex. This review will discuss results obtained by studies on the effects of experience on the development of coping strategies and on the neurobiological mediators of these effects, focusing on those studies that tested the moderator influence of genotype, sex, or both. The studies reported were chosen because they offered data on the effects of genotype, sex, or their interaction
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
