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Abnormal brain structure and behavior in MyD88-deficient mice.

Patricia Schroeder1, Marion Rivalan2, Sami Zaqout3

  • 1Institute of Cell Biology and Neurobiology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.

Brain, Behavior, and Immunity
|October 1, 2020
PubMed

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Summary

Myeloid differentiation primary response protein 88 (MyD88) deficiency impacts mouse brain development and adult structure, altering neuronal density, arborization, and myelinization. These changes correlate with specific behavioral modifications, suggesting MyD88

Area of Science:

  • Neuroscience
  • Immunology
  • Developmental Biology

Background:

  • Toll-like receptors (TLRs) and IL-1R family signaling are crucial in host defense and development.
  • The role of these pathways, particularly the adaptor protein myeloid differentiation primary response protein 88 (MyD88), in mammalian brain development is largely unknown.

Purpose of the Study:

  • To investigate the impact of MyD88 deficiency on murine brain structure during development and in adulthood.
  • To assess the behavioral consequences of MyD88 deficiency in mice.

Main Methods:

  • Systematic investigation of Myd88 knockout (Myd88-/-) mice compared to wild-type littermates.
  • Analysis of brain structure (neocortical thickness, neuronal density, cell numbers, arborization, myelinization) at neonatal and adult stages.
Keywords:
Brain developmentMouse behaviorMyD88NeocortexTollToll-like receptors

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  • Behavioral testing including locomotor activity, anxiety, learning, and memory.

    • Main Results:

    • Neonatal Myd88-/- mice showed reduced neocortical thickness and increased neuronal density.
    • Adult Myd88-/- mice exhibited increased neuronal density, reduced arborization, enhanced myelinization, and altered glial and proliferating cell numbers.
    • Behavioral analysis revealed decreased locomotor activity, increased anxiety, potential cognitive inflexibility, but normal learning and memory.

    Conclusions:

    • MyD88 deficiency leads to significant morphologic and cellular alterations in the developing and adult mouse brain.
    • These structural changes are associated with distinct behavioral phenotypes.
    • The findings highlight a pathophysiological role for MyD88 in mammalian central nervous system development, structure, and function.