Classical MHCI Molecules Regulate Retinogeniculate Refinement and Limit Ocular Dominance Plasticity

Akash Datwani, Michael J. McConnell, Patrick O. Kanold, Kristina D. Micheva, Brad Busse, Mehrdad Shamloo, Stephen J. Smith, Carla J. Shatz

Research output: Contribution to journalArticlepeer-review

150 Scopus citations


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-Kb and H2-Db, ocular dominance (OD) plasticity is enhanced. Mice lacking PirB, an MHCI receptor, have a similar phenotype. H2-Kb and H2-Db are 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-Kb and H2-Db can account for observed changes in synapse plasticity. H2-Kb and H2-Db ligands, signaling via neuronal MHCI receptors, may enable activity-dependent remodeling of brain circuits during developmental critical periods.

Original languageEnglish (US)
Pages (from-to)463-470
Number of pages8
Issue number4
StatePublished - Nov 25 2009
Externally publishedYes



ASJC Scopus subject areas

  • Neuroscience(all)


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