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Constitutive knockout of the membrane cytoskeleton protein beta adducin decreases mushroom spine density in the nucleus accumbens but does not prevent spine remodeling in response to cocaine
Author(s) -
Jung Yonwoo,
Mulholland Patrick J.,
Wiseman Shari L.,
Judson Chandler L.,
Picciotto Marina R.
Publication year - 2013
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/ejn.12037
Subject(s) - dendritic spine , nucleus accumbens , synaptic plasticity , chemistry , spine (molecular biology) , medicine , endocrinology , knockout mouse , mushroom bodies , neuroplasticity , neuroscience , biology , microbiology and biotechnology , central nervous system , hippocampal formation , biochemistry , drosophila melanogaster , gene , receptor
The adducin family of proteins associates with the actin cytoskeleton in a calcium‐dependent manner. Beta adducin (β A dd) is involved in synaptic plasticity in the hippocampus; however, the role of β A dd in synaptic plasticity in other brain areas is unknown. Using diolistic labeling with the lipophilic dye D i I , we found that the density of mature mushroom‐shaped spines was significantly decreased in the nucleus accumbens ( NA c) in brain slices from β A dd‐knockout ( KO ) mice as compared to their wildtype ( WT ) siblings. The effect of 10 days of daily cocaine (15 mg/kg) administration on NA c spine number and locomotor behavior was also measured in β A dd WT and KO mice. As expected, there was a significant increase in overall spine density in NA c slices from cocaine‐treated WT mice at this time‐point; however, there was a greater increase in the density of mushroom spines in β A dd‐ KO animals following chronic cocaine administration than in WT . In addition, β A dd‐ KO mice showed elevated locomotor activity in response to cocaine treatment compared to WT siblings. These results indicate that β A dd is required for stabilising mature spines under basal conditions in the NA c, but that lack of this protein does not prevent synaptic remodeling following repeated cocaine administration. In addition, these data are consistent with previous studies suggesting that β A dd may normally be involved in stabilising spines once drug‐ or experience‐dependent remodeling has occurred.