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Rab‐Mediated Endocytosis
Author(s) -
BASKYS ANDRIUS,
BAYAZITOV ILDAR,
ZHU ERCHENG,
FANG LIWEI,
WANG RONG
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1403.023
Subject(s) - neuroprotection , rab , metabotropic glutamate receptor , neuroscience , neurotransmission , synaptic plasticity , biology , long term depression , glutamate receptor , gtpase , microbiology and biotechnology , ampa receptor , receptor , biochemistry
Rab proteins are small GTPases involved in endocytosis and recycling of cell surface molecules. Recently they have been implicated in the etiopathogenesis of several neurodegenerative disorders including Alzheimer's and Lewy body disease. In experiments on organotypic hippocampal cultures, upregulation of Rab protein family member Rab5b after group I metabotropic glutamate receptor (mGluR) stimulation was associated with reduced neuronal vulnerability to excitotoxic injury. This mGluR‐mediated neuroprotection was abolished by antisense‐induced deficiency of Rab5b. Electrophysiological measurements of excitatory synaptic transmission in the Schaffer collateral–CA1 pathway revealed that mGluR activation that induces neuroprotection also induced long‐term depression (LTD) of synaptic transmission. Similar to the neuroprotection, Rab5b deficiency abolished dihydroxyphenylglycine‐induced LTD. Together, these findings support the idea that Rab proteins, and the Rab5b protein in particular, may provide a link between neurodegenerative disease, neuroprotection, and synaptic plasticity, as well as possibly being a useful target for pharmacological interventions.