A self-medication hypothesis for increased vulnerability to drug abuse in prenatally restraint stressed rats

Marie Line Reynaert, Jordan Marrocco, Eleonora Gatta, Jérôme Mairesse, Gilles Van Camp, Francesca Fagioli, Stefania Maccari, Ferdinando Nicoletti, Sara Morley-Fletcher

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Stress-related events that occur in the perinatal period can permanently change brain and behavior of the developing individual and there is increasing evidence that early-life adversity is a contributing factor in the etiology of drug abuse and mood disorders. Neural adaptations resulting from early-life stress may mediate individual differences in novelty responsiveness and in turn contribute to drug abuse vulnerability. Prenatal restraint stress (PRS) in rats is a well-documented model of early stress known to induce long-lasting neurobiological and behavioral alterations including impaired feedback mechanisms of the HPA axis, enhanced novelty seeking, and increased sensitiveness to psychostimulants as well as anxiety/ depression-like behavior. Together with the HPA axis, functional alterations of the mesolimbic dopamine system and of the metabotropic glutamate receptors system appear to be involved in the addiction-like profile of PRS rats.

Original languageEnglish
Title of host publicationAdvances in Neurobiology
PublisherSpringer New York LLC
Pages101-120
Number of pages20
Volume10
DOIs
Publication statusPublished - 2015

Publication series

NameAdvances in Neurobiology
Volume10
ISSN (Print)02700794

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience
  • Developmental Neuroscience
  • Neurology

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  • Cite this

    Reynaert, M. L., Marrocco, J., Gatta, E., Mairesse, J., Van Camp, G., Fagioli, F., Maccari, S., Nicoletti, F., & Morley-Fletcher, S. (2015). A self-medication hypothesis for increased vulnerability to drug abuse in prenatally restraint stressed rats. In Advances in Neurobiology (Vol. 10, pp. 101-120). (Advances in Neurobiology; Vol. 10). Springer New York LLC. https://doi.org/10.1007/978-1-4939-1372-5_6