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Classical MHCI molecules regulate retinogeniculate refinement and limit ocular dominance plasticity.

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-K(b) and H2-D(b), ocular dominance (OD) plasticity is enhanced. Mice lacking PirB, an MHCI receptor, have a similar phenotype. H2-K(b) and H2-D(b) 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 K(b)D(b-/-) mice, developmental refinement of retinogeniculate projections is impaired, similar to C1q(-/-) mice. These phenotypes in K(b)D(b-/-) mice are strikingly similar to those in beta2 m(-/-)TAP1(-/-) mice, which lack cell surface expression of all MHCIs, implying that H2-K(b) and H2-D(b) can account for observed changes in synapse plasticity. H2-K(b) and H2-D(b) ligands, signaling via neuronal MHCI receptors, may enable activity-dependent remodeling of brain circuits during developmental critical periods.

Pubmed ID: 19945389

Authors

  • Datwani A
  • McConnell MJ
  • Kanold PO
  • Micheva KD
  • Busse B
  • Shamloo M
  • Smith SJ
  • Shatz CJ

Journal

Neuron

Publication Data

November 25, 2009

Associated Grants

  • Agency: NEI NIH HHS, Id: F32 EY013526
  • Agency: NEI NIH HHS, Id: F32 EY013526-01
  • Agency: NEI NIH HHS, Id: R01 EY002858
  • Agency: NEI NIH HHS, Id: R01 EY002858-33
  • Agency: NEI NIH HHS, Id: R01 EY02858
  • Agency: NIMH NIH HHS, Id: R01 MH071666
  • Agency: NIMH NIH HHS, Id: R01 MH071666
  • Agency: NIMH NIH HHS, Id: R01 MH071666-06
  • Agency: NCI NIH HHS, Id: T32CA09361

Mesh Terms

  • Animals
  • Animals, Newborn
  • Dominance, Ocular
  • Geniculate Bodies
  • H-2 Antigens
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Mutant Strains
  • Neuroimmunomodulation
  • Neuronal Plasticity
  • Retina
  • Visual Pathways