机构：[a]Memory Disorders Program, VA HCS Long Beach, Long Beach, California, USA[b]Southern California Institute for Research and Education (SCIRE), Long Beach, California, USA[c]Psychiatry and Human Behavior, University of California at Irvine, Irvine, California, USA[d]Present address: Department of Developmental Neurobiology, St. Jude Children’s Research Hospital, Memphis, Tennessee, USA.[e]Experimental Center, Xuan-wu Hospital of Capital Medical University, Key Laboratory for Neurodegenerative Diseases of Ministry of Education, Beijing, China神经变性病教育部重点实验室首都医科大学宣武医院[f]Present address: Experimental Center, Xuan-wu Hospital of Capital Medical University, Key Laboratory for Neurodegenerative Diseases of Ministry of Education, Beijing, China.神经变性病教育部重点实验室首都医科大学宣武医院
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.
基金：
Southern California Institute for Research and Education (SCIRE) and VISN22 Mental Illness Research and Education Clinical Centre (MIRECC).
第一作者机构：[a]Memory Disorders Program, VA HCS Long Beach, Long Beach, California, USA[b]Southern California Institute for Research and Education (SCIRE), Long Beach, California, USA[c]Psychiatry and Human Behavior, University of California at Irvine, Irvine, California, USA[*]Memory Disorders Program, VA HCS Long Beach, 5901 E. 7th St. 06/116 A, Long Beach, CA 90822.
通讯作者：
通讯机构：[*]Memory Disorders Program, VA HCS Long Beach, 5901 E. 7th St. 06/116 A, Long Beach, CA 90822.
推荐引用方式(GB/T 7714)：
ANDRIUS BASKYS ,ILDAR BAYAZITOV ,ERCHENG ZHU ,et al.Rab-mediated endocytosis - Linking neurodegeneration, neuroprotection, and synaptic plasticity?[J].ANNALS OF THE NEW YORK ACADEMY OF SCIENCES.2007,1122:313-329.doi:10.1196/annals.1403.023.
APA：
ANDRIUS BASKYS,,ILDAR BAYAZITOV,,ERCHENG ZHU,,LIWEI FANG,&RONG WANG.(2007).Rab-mediated endocytosis - Linking neurodegeneration, neuroprotection, and synaptic plasticity?.ANNALS OF THE NEW YORK ACADEMY OF SCIENCES,1122,
MLA：
ANDRIUS BASKYS,,et al."Rab-mediated endocytosis - Linking neurodegeneration, neuroprotection, and synaptic plasticity?".ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 1122.(2007):313-329
