Peer-Reviewed Journal Details
Mandatory Fields
Adelson, J. D.,Barreto, G. E.,Xu, L.,Kim, T.,Brott, B. K.,Ouyang, Y. B.,Naserke, T.,Djurisic, M.,Xiong, X.,Shatz, C. J.,Giffard, R. G.
2012
March
Neuronneuron
Neuroprotection from stroke in the absence of MHCI or PirB
Published
()
Optional Fields
Animals Astrocytes/pathology Biotin/analogs & derivatives Brain/metabolism Calcium-Binding Proteins/metabolism Dextrans Disease Models, Animal Gene Expression Regulation/*genetics Glial Fibrillary Acidic Protein/metabolism Histocompatibility Antigens Class I/genetics/*metabolism Infarction, Middle Cerebral Artery/pathology/*physiopathology Mice Mice, Inbred C57BL Mice, Knockout Microfilament Proteins/metabolism Motor Activity/genetics Motor Cortex/pathology Organ Culture Techniques Phosphopyruvate Hydratase/metabolism Pyramidal Tracts/pathology Receptors, Immunologic/*deficiency/genetics Recovery of Function/*genetics Signal Transduction/genetics Time Factors
73
66
1100
7
Recovery from stroke engages mechanisms of neural plasticity. Here we examine a role for MHC class I (MHCI) H2-Kb and H2-Db, as well as PirB receptor. These molecules restrict synaptic plasticity and motor learning in the healthy brain. Stroke elevates neuronal expression not only of H2-Kb and H2-Db, but also of PirB and downstream signaling. KbDb knockout (KO) or PirB KO mice have smaller infarcts and enhanced motor recovery. KO hippocampal organotypic slices, which lack an intact peripheral immune response, have less cell death after in vitro ischemia. In PirB KO mice, corticospinal projections from the motor cortex are enhanced, and the reactive astrocytic response is dampened after MCAO. Thus, molecules that function in the immune system act not only to limit synaptic plasticity in healthy neurons, but also to exacerbate brain injury after ischemia. These results suggest therapies for stroke by targeting MHCI and PirB.Recovery from stroke engages mechanisms of neural plasticity. Here we examine a role for MHC class I (MHCI) H2-Kb and H2-Db, as well as PirB receptor. These molecules restrict synaptic plasticity and motor learning in the healthy brain. Stroke elevates neuronal expression not only of H2-Kb and H2-Db, but also of PirB and downstream signaling. KbDb knockout (KO) or PirB KO mice have smaller infarcts and enhanced motor recovery. KO hippocampal organotypic slices, which lack an intact peripheral immune response, have less cell death after in vitro ischemia. In PirB KO mice, corticospinal projections from the motor cortex are enhanced, and the reactive astrocytic response is dampened after MCAO. Thus, molecules that function in the immune system act not only to limit synaptic plasticity in healthy neurons, but also to exacerbate brain injury after ischemia. These results suggest therapies for stroke by targeting MHCI and PirB.
1097-4199 (Electronic) 08
2012/03/27
http://www.ncbi.nlm.nih.gov/pubmed/22445338http://www.ncbi.nlm.nih.gov/pubmed/22445338
10.1016/j.neuron.2012.01.020
Grant Details