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Protein aggregation in postsynaptic density after transient brain ischemia
Author(s) -
Beręsewicz M.,
Zabłocka B.,
DomańskaJanik K.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.85.s2.16_3.x
Subject(s) - postsynaptic density , postsynaptic potential , excitatory postsynaptic potential , microbiology and biotechnology , neurotransmission , neurotransmitter receptor , glutamate receptor , scaffold protein , signal transduction , neuroscience , nmda receptor , biophysics , cytoskeleton , receptor , signal transducing adaptor protein , chemistry , biology , biochemistry , cell
Brief cerebral ischemia causes changes in synaptic transmission and in consequence in neuronal function manifested in delayed cell death of CA1 hippocampal region. Postsynaptic density (PSD) is composed by a network of interacting proteins, including scaffolding proteins, neurotransmitter receptors, cytoskeletal proteins and protein kinases. PSD dynamically modulates signal transduction what influence the cell fate. We investigated the composition of the PSD network and effect of ischemia on its complexity. Two experimental procedures were applied. The interaction between PSD‐95 and Src, Fyn, Raf‐1, paxilin or NMDA receptor subunits were explored using coimmunoprecipitation method. In addition, the effect of ischemia‐reperfusion on the density of PSD were evaluated by measurement of is solubility. We find out the decrease in solubility of the PSD‐95, NR2A, NR2B and Raf‐1. Of interest, the latter was restricted to surviving regions of hippocampus. Acknowledgement: Financed by PBZ‐KBN‐002/CD/P05/2000.