NMDA-type glutamate receptors play a critical role in the activity-dependent development and structural remodeling of dendritic arbors and spines. However, the molecular mechanisms that link NMDA receptor activation to changes in dendritic morphology remain unclear. We report that the Rac1-GEF Tiam1 is present in dendrites and spines and is required for their development. Tiam1 interacts with the NMDA receptor and is phosphorylated in a calcium-dependent manner in response to NMDA receptor stimulation. Blockade of Tiam1 function with RNAi and dominant interfering mutants of Tiam1 suggests that Tiam1 mediates effects of the NMDA receptor on dendritic development by inducing Rac1-dependent actin remodeling and protein synthesis. Taken together, these findings define a molecular mechanism by which NMDA receptor signaling controls the growth and morphology of dendritic arbors and spines.
The Rac1-GEF Tiam1 couples the NMDA receptor to the activity-dependent development of dendritic arbors and spines. Publishing Authors By Initials
The Rac1-GEF Tiam1 couples the NMDA receptor to the activity-dependent development of dendritic arbors and spines. Journal Published:
PUBLICATION TYPE: Research Support, U.S. Gov't,
Journal: Neuron
VOLUME: 45
Page Numbers: 525-38
Journal Abbreviation: Neuron
ISSN: 0896-6273
DAY: 17
MONTH: Feb
YEAR: 2005
The Rac1-GEF Tiam1 couples the NMDA receptor to the activity-dependent development of dendritic arbors and spines. Information
Number of References:
LANGUAGE: eng
NlmUniqueID: 8809320
The Rac1-GEF Tiam1 couples the NMDA receptor to the activity-dependent development of dendritic arbors and spines. Keywords Mesh Terms:
KEYWORDS: rac1 GTP-Binding Protein
MESH TERMS: metabolism
Chemical & Substance for Abstract: The Rac1-GEF Tiam1 couples the NMDA receptor to the activity-dependent development of dendritic arbors and spines. Information
Substance Name: rac1 GTP-Binding Protein
Registry Number: EC 3.6.5.2
Grant and Affiliation Information for The Rac1-GEF Tiam1 couples the NMDA receptor to the activity-dependent development of dendritic arbors and spines.
AFFILIATION: Neurobiology Program, Children's Hospital, Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA.
Country: United States
AGENCY: United States NICHD
GRANT: P30-HD18655
ACRONYM: HD
MEDLINETA: Neuron
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