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Neuron. 2009 Nov 25;64(4):463-70. doi: 10.1016/j.neuron.2009.10.015.

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

Author information

1
Departments of Biology, James H. Clark Center, Stanford University, Stanford, CA 94305, USA.

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-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.

PMID:
19945389
PMCID:
PMC2787480
DOI:
10.1016/j.neuron.2009.10.015
[Indexed for MEDLINE]
Free PMC Article

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