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Adolescent stress during, but not after, pubertal onset impairs indices of prepulse inhibition in adult rats.

Carly M DrzewieckiJari WillingLaura R CortesJanice M Juraska
Published in: Developmental psychobiology (2021)
Exposure to stress during adolescence is a risk factor for developing several psychiatric disorders, many of which involve prefrontal cortex (PFC) dysfunction. The human PFC and analogous rodent medial prefrontal cortex (mPFC) continue to mature functionally and anatomically during adolescence, and some of these maturational events coincide with pubertal onset. As developing brain regions are more susceptible to the negative effects of stress, this may make puberty especially vulnerable. To test this, we exposed male and female rats to isolation and restraint stress during the onset of puberty or during the post-pubertal period of adolescence. In young adulthood, both stressed groups and an unstressed control group underwent testing on a battery of tasks to assess emotional and cognitive behaviors, and the volume of the mPFC was quantified postmortem. Factor analysis revealed only subjects stressed peri-pubertally showed a long-term deficiency compared to controls in prepulse inhibition. Additionally, both sexes showed volumetric mPFC decreases following adolescent stress, and these losses were most pronounced in females. Our findings suggest that pubertal onset may be a vulnerable window wherein adolescents are most susceptible to the negative consequences of stress exposure. Furthermore, it highlights the importance of accounting for pubertal status when studying adolescents.
Keyphrases
  • prefrontal cortex
  • young adults
  • depressive symptoms
  • stress induced
  • physical activity
  • endothelial cells
  • heat stress
  • brain injury
  • blood brain barrier
  • resting state