Functional requirement for class I MHC in CNS development and plasticity.

By G. S. Huh, L. Boulanger, H. Du, P. A. Riquelme, T. Brotz, C. Shatz. Science, 2000

843 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/a1a2692f8fc684aea21c0f61a22a08f669efc2dd

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In Cellular and Molecular Neuroscience

In Immunology

In Neurology

Citations in the corpus

The complement system: an unexpected role in synaptic pruning during development and disease. (2012, background): “Moreover, animals deficient in MHC-I molecules have defects in eye-specific segregation in the retinogeniculate pathway and ocular dominance plasticity, suggesting a role in developmental elimination of CNS synapses (Huh et al. 2000, Syken et al. 2006).”
Autism and Abnormal Development of Brain Connectivity (2004, background): “Decreased expression of MHC class I impairs the pruning of inappropriate synaptic connections (Huh et al., 2000), an effect that may explain the early developmental increase in brain volume in autism and the symptomatic overlap with FXS.”
The Aging Astrocyte Transcriptome from Multiple Regions of the Mouse Brain (2018, background): “, 2012), although, in the developing brain, MHC class I plays a role in promoting synapse elimination (Huh et al., 2000).”
Cytokines and CNS development. (2009, positive): “and hippocampus, but also in distinct neuronal populations throughout the CNS (Huh et al., 2000), raising the possibility that class I MHC signaling is involved in the synaptic refinement of additional circuits.”
The mystery and magic of glia: a perspective on their roles in health and disease. (2008, background): “These findings add to the growing evidence that immune system molecules are crucial for the patterning of neural circuits (Boulanger and Shatz, 2004; Huh et al., 2000) and support a model in which unwanted synapses are tagged by complement proteins for elimination by phagocytic cells.”
Critical period regulation. (2004, background): “Signaling by major histocompatibility complex (MHC)–related molecules is important (Huh et al. 2000).”
Immune activation in brain aging and neurodegeneration: too much or too little? (2009, background): “…highlighting the role of ''immune molecules'' such as complement and class I major histocompatibility complex in CNS development and plasticity (Huh et al., 2000; Stevens et al., 2007; and see review article in this issue by Boulanger [2009]) or ''CNS factors'' such as neurotransmitters in…”
Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, positive): “Specifically, mice with genetic deficiency of MHC-I or the MHC-I receptor component, CD3f, display enhanced LTP and an absence of LTD in the hippocampus (Boulanger and Shatz, 2004; Huh et al., 2000), as well as lower threshold for induction of LTD in the cerebellum, associated with improved motor le”
A role for correlated spontaneous activity in the assembly of neural circuits (2013, positive): “Knockout of molecules associated with MHC1 signaling (Datwani et al., 2009; Huh et al., 2000; Syken et al., 2006) Normal retinal waves Unknown Reduced segregation NP1/2 KO mouse (lacks neuronal pentraxins NP1/2) (Bjartmar et al., 2006; Koch and Ullian, 2010)”
The role of adult hippocampal neurogenesis in brain health and disease (2018, background): “1 molecule, which is involved in synaptic plasticity [100, 101], were also identified as an aging-dependent negative”