title: Activation of N-methyl-D-aspartate receptor induces a shift of drebrin distribution: disappearance from dendritic spines and appearance in dendritic shafts.
abstract: Drebrin is a major actin-filament-binding protein localized in mature dendritic spines. A recent in vivo immunoelectron microscopic study suggests that drebrin content at each dendritic spine is regulated by some unknown mechanisms. In the present in vitro study, we examined whether glutamate stimulation alters drebrin content in dendritic spines. Glutamate stimulation induced disappearance of drebrin immunostaining from dendritic spines but led to appearance of drebrin immunostaining in dendritic shafts and somata. The glutamate-induced shift of drebrin immunostaining was blocked by an NMDA receptor antagonist. Immunoblot analyses showed that both the total and the cytosolic drebrin remained unchanged and revealed that the drebrin shift was not due to drebrin degradation. These findings indicate that NMDA receptor activation induces a shift in subcellular distribution of drebrin associated with actin filaments, and that the shift might be a molecular basis for actin reorganization accompanied with synaptic plasticity.
authors.affiliation: Department of Neurobiology and Behavior, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma 371-8511, Japan.
authors.forename: Yuko
authors.initials: Y
authors.lastname: Sekino
authors.forename: Satoshi
authors.initials: S
authors.lastname: Tanaka
authors.forename: Kenji
authors.initials: K
authors.lastname: Hanamura
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yamazaki
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Sasagawa
authors.forename: Yinhuan
authors.initials: Y
authors.lastname: Xue
authors.forename: Kensuke
authors.initials: K
authors.lastname: Hayashi
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Shirao
mesh_terms: D008841:Actin Cytoskeleton / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D001921:Brain / Q000166:cytology / Q000378:metabolism*; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism; D018920:Coculture Techniques; D003600:Cytosol / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D049229:Dendritic Spines / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D007150:Immunohistochemistry; D018613:Microscopy, Confocal; D009457:Neuroglia / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009479:Neuropeptides / Q000378:metabolism*; D021381:Protein Transport / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000378:metabolism*; D013570:Synaptic Membranes / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
chemical_list: D018691:Excitatory Amino Acid Antagonists; D009479:Neuropeptides; D016194:Receptors, N-Methyl-D-Aspartate; C053386:drebrins; D018698:Glutamic Acid