Classical MHCI Molecules Regulate Retinogeniculate Refinement and Limit Ocular Dominance Plasticity

  • Datwani A
  • McConnell M
  • Kanold P
 et al. 
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Abstract

Major histocompatibility complex class I (MHCI) genes were discovered unexpectedly in healthy CNS neurons in a screen for genes regulated by neural activity. In mice lacking just 2 of the 50+ MHCI genes H2-Kband H2-Db, ocular dominance (OD) plasticity is enhanced. Mice lacking PirB, an MHCI receptor, have a similar phenotype. H2-Kband H2-Dbare expressed not only in visual cortex, but also in lateral geniculate nucleus (LGN), where protein localization correlates strongly with synaptic markers and complement protein C1q. In KbDb-/-mice, developmental refinement of retinogeniculate projections is impaired, similar to C1q-/-mice. These phenotypes in KbDb-/-mice are strikingly similar to those in β2 m-/-TAP1-/-mice, which lack cell surface expression of all MHCIs, implying that H2-Kband H2-Dbcan account for observed changes in synapse plasticity. H2-Kband H2-Dbligands, signaling via neuronal MHCI receptors, may enable activity-dependent remodeling of brain circuits during developmental critical periods. © 2009 Elsevier Inc. All rights reserved.

Author-supplied keywords

  • MOLIMMUNO
  • MOLNEURO
  • SIGNALING

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Authors

  • Akash Datwani

  • Michael J. McConnell

  • Kristina D. Micheva

  • Brad Busse

  • Mehrdad Shamloo

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