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Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Developmental Neurobiology

Background:

  • Postsynaptic density protein-95 (PSD-95) is crucial for excitatory synapse maturation, regulating N-methyl-D-aspartic acid receptors (NMDAR) and α-amino-3-hydroxy-5-methyl-4-isox-azoleproprionic acid receptors (AMPAR) trafficking.
  • PSD-95 disruption is linked to neuropsychiatric disorders like schizophrenia and autism.
  • The impact of PSD-95 deficiency on prefrontal cortex (PFC) functions, including cognition, working memory, and sociability, remains largely unexplored.

Purpose of the Study:

  • To investigate the effects of PSD-95 deficiency on NMDAR and AMPAR expression and function in the medial prefrontal cortex (mPFC).
  • To examine the behavioral consequences of PSD-95 deficiency on cognition, working memory, and sociability in a mouse model.
  • To assess these effects during critical juvenile and adolescent developmental periods.

Main Methods:

  • Utilized a PSD-95 knockout mouse model (PSD-95-/-).
  • Analyzed NMDAR and AMPAR subunit expression and function in the mPFC.
  • Conducted behavioral tests to assess sociability, learning, and working memory.

Main Results:

  • PSD-95-/- mice showed increased NMDAR subunits (GluN1, GluN2B) and decreased AMPAR subunit (GluA1) protein levels during adolescence.
  • An elevated NMDAR/AMPAR current amplitude ratio was observed, progressing from juvenile to adolescent stages.
  • Behaviorally, PSD-95-/- mice exhibited deficits in sociability, learning, and working memory.

Conclusions:

  • PSD-95 deficiency disrupts mPFC synaptic function and associated behaviors during critical neurodevelopmental stages.
  • These findings underscore the importance of PSD-95 in mPFC development.
  • The study suggests a potential link between PSD-95 dysfunction and the pathogenesis of schizophrenia and/or autism.