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Intact corticostriatal function in aged system xc- - deficient mice.

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Aged mice lacking the xCT transporter show restored corticostriatal neurotransmission and social behavior, unlike young adults. This suggests xCT deficiency may protect against age-related brain changes.

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Area of Science:

  • Neuroscience
  • Neurochemistry
  • Aging Research

Background:

  • System xc- (cystine/glutamate antiporter) influences striatal glutamate levels and corticostriatal neurotransmission.
  • Previous studies showed xCT deficiency in young mice leads to impaired neurotransmission and autism spectrum disorder (ASD)-like behaviors.
  • Atypical brain aging is linked to ASD, but xCT-/- mice exhibit protection against hippocampal aging.

Purpose of the Study:

  • To investigate if corticostriatal impairments and ASD-like behaviors persist in aged xCT-/- mice.
  • To determine the impact of xCT deletion on aged corticostriatal synapses and neurotransmission.
  • To assess age-related changes in behavior and brain pathology in the absence of xCT.

Main Methods:

  • Comparison of neurotransmission, synaptic ultrastructure, and intracellular glutamate levels in aged (16-month-old) xCT-/- and wildtype (xCT+/+) mice.
  • Behavioral testing including repetitive and social interaction assays in aged mice.
  • Analysis of advanced glycation end-products in striatal tissue.

Main Results:

  • Corticostriatal neurotransmission and medium-spiny neuron morphology were unaffected in aged xCT-/- mice.
  • Synaptic ultrastructure and intracellular glutamate levels were largely unaltered in aged xCT-/- mice.
  • Repetitive and social behaviors were comparable between aged groups, with xCT-/- mice showing fewer aggressive/dominant interactions.

Conclusions:

  • Corticostriatal and social behavior impairments observed in young xCT-/- mice are resolved in aged mice.
  • Restored intracellular glutamate levels likely account for the normalization of neurotransmission and behavior.
  • Reduced advanced glycation end-products in xCT-/- mice may confer protection against age-related brain pathology.