Animal Models of the Impact of Social Stress on Cocaine Use Disorders

Int Rev Neurobiol. 2018:140:131-169. doi: 10.1016/bs.irn.2018.07.005. Epub 2018 Aug 20.

Abstract

Cocaine use disorders are strongly influenced by the social conditions prior, during, and after exposure to cocaine. In this chapter, we discuss how social factors such as early life stress, social rank stress, and environmental stress impact vulnerability and resilience to cocaine. The discussion of each animal model begins with a brief review of examples from the human literature, which provide the psychosocial background these models attempt to capture. We then discuss preclinical findings from use of each model, with emphasis on how social factors influence cocaine-related behaviors and how sex and age influence the behaviors and neurobiology. Models discussed include (1) early life social stress, such as maternal separation and neonatal isolation, (2) social defeat stress, (3) social hierarchies, and (4) social isolation and environmental enrichment. The cocaine-related behaviors reviewed for each of these animal models include cocaine-induced conditioned place preference, behavioral sensitization, and self-administration. Together, our review suggests that the degree of psychosocial stress experienced yields robust effects on cocaine-related behaviors and neurobiology, and these preclinical findings have translational impact for the future of cocaine use disorder treatment.

Keywords: Cocaine-related disorders; Disease models; Hierarchy; Neurobiology; Social isolation; Stress; animal; psychological; social.

Publication types

  • Review

MeSH terms

  • Animals
  • Behavior, Animal / physiology*
  • Cocaine-Related Disorders* / etiology
  • Cocaine-Related Disorders* / metabolism
  • Cocaine-Related Disorders* / physiopathology
  • Disease Models, Animal*
  • Humans
  • Maternal Deprivation*
  • Social Behavior*
  • Social Environment*
  • Stress, Psychological* / complications
  • Stress, Psychological* / metabolism
  • Stress, Psychological* / physiopathology