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Social experience in adolescence shapes prefrontal cortex structure and function in adulthood.

Dan C Li1,2, Elizabeth A Hinton3,4, Jidong Guo3,5

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Adolescent isolation in mice leads to lasting habit-like behaviors and reward deficits. These changes are linked to overactive ventromedial prefrontal cortex (vmPFC) circuits, highlighting a critical period for social influence on brain development.

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Behavioral Science

Background:

  • Adolescence is a critical period for prefrontal cortex (PFC) development.
  • Social environment significantly impacts PFC maturation and can influence psychopathology.
  • Disruptions during this period may have long-lasting neurobehavioral consequences.

Purpose of the Study:

  • To investigate the long-term neurobehavioral effects of adolescent isolation in mice.
  • To identify the underlying neural mechanisms in the ventromedial PFC (vmPFC).
  • To explore the role of cytoskeletal regulatory pathways in these long-term changes.

Main Methods:

  • Mice were subjected to social isolation during adolescence.
  • Neurobehavioral assessments were conducted to evaluate habit formation, goal-directed behavior, and anhedonia.
  • Electrophysiological recordings and molecular analyses were performed on the vmPFC.
  • Interventions targeting cytoskeletal pathways were employed.

Main Results:

  • Adolescent isolation induced persistent habit-like behaviors and anhedonia-like deficits.
  • These behavioral changes were associated with dendritic spine over-abundance and hyper-excitability in the vmPFC.
  • vmPFC hyperactivity was both necessary and sufficient for isolation-induced behavioral inflexibility.
  • Isolation activated specific cytoskeletal pathways, and their repression prevented long-term neurobiological changes.

Conclusions:

  • Adolescence represents a critical period for social influence on PFC maturation.
  • Social isolation during adolescence can establish long-lasting neurobiological alterations in the vmPFC.
  • These alterations contribute to behavioral inflexibility and reward deficits, potentially priming for psychopathology.
  • Targeting specific molecular pathways may offer therapeutic avenues for mitigating the effects of early-life adversity.