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Rac1‐dependent actin remodeling as a molecular mechanism shaping spine density
Author(s) -
Bongmba Odelia Yuh Ngala,
Tejada-Simon Maria Victoria
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb692
Subject(s) - dendritic spine , neuroscience , rac1 , biology , spine (molecular biology) , hippocampus , actin remodeling , actin , actin cytoskeleton , synaptic plasticity , microbiology and biotechnology , actin remodeling of neurons , morphogenesis , phenotype , cofilin , cytoskeleton , signal transduction , cell , hippocampal formation , genetics , receptor , gene
Abnormal dendritic spine morphogenesis has been associated with several psychiatric conditions linked to autism. A consistent abnormality observed in the brain of some of these patients and animal models is related to neurons showing a high density of long, thin, immature spines. Although these abnormalities have been correlated with impaired cognitive abilities in autistic and other syndromes, the causes of these malformations are not yet well understood. The formation and maintenance of dendritic spines require a very dynamic actin cytoskeleton, regulated by small GTPases such as Rac1. Previously, by creating a tissue‐specific Rac1 deficient mouse, our laboratory reported that Rac1 is (1) necessary for normal dendritic and spine development, (2) critical for hippocampus‐dependent learning and memory, and (3) essential for long‐term plasticity. Following up our previous findings, herein we demonstrate that ablation of Rac1 indeed leads to reduced spine density and altered actin remodeling pathway. Thus, regulation of Rac1 may provide a functional link among deficient neuronal morphology, aberrant synaptic plasticity and cognition impairment, phenotypes associated with certain autistic disorders.