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P2‐288: Abeta‐mediated glutamate release from astrocytes
Author(s) -
Sanz-Blasco Sara,
Piña-Crespo Juan,
Talantova Maria,
Lipton Stuart
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.05.1338
Subject(s) - glutamate receptor , excitotoxicity , förster resonance energy transfer , microbiology and biotechnology , nmda receptor , metabotropic glutamate receptor 6 , chemistry , metabotropic glutamate receptor , neuroligin , biophysics , hek 293 cells , neurotransmission , astrocyte , metabotropic glutamate receptor 5 , biology , neuroscience , biochemistry , receptor , fluorescence , central nervous system , excitatory postsynaptic potential , physics , quantum mechanics
pharmacotherapy may complement current therapies. Hence, we aim to investigate the distribution of CB1 in the cortex of AD and controls and correlates with clinical features. Methods: Postmortem brain tissues samples of subjects were obtained from established longitudinal studies with prospectively obtained clinical data. Blocks of thawed tissue from brain areas (BA 9, BA 17, hippocampus, anterior cingulate and caudate) were dissected free of white matter, washed and processed for experiments. Immunoblotting was used to measure protein expression. CB1 receptor function was characterized by means of the [3H]SR141716A saturation binding assay. Results: There are no significant CB1 density changes between AD (n1⁄4 15) and controls (n1⁄4 14). The distribution of CB1 density was: BA9 < Caudate < Hippocampus