scholarly journals Corrigendum to: Regional Differences in Brain-Derived Neurotrophic Factor Levels and Dendritic Spine Density Confer Resilience to Inescapable Stress

2021 ◽  
Keyword(s):  
Dendritic Spine ◽  
Neurotrophic Factor ◽  
Regional Differences ◽  
Brain Derived Neurotrophic Factor ◽  
Spine Density ◽  
Dendritic Spine Density

Regional differences in dendritic spine density confer resilience to chronic social defeat stress

2017 ◽  
Vol 30 (2) ◽  
pp. 117-122 ◽  
Author(s):  
Youge Qu ◽  
Chun Yang ◽  
Qian Ren ◽  
Min Ma ◽  
Chao Dong ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Regional Differences ◽  
Social Defeat ◽  
Brain Regions ◽  
Control Group ◽  
Spine Density ◽  
Dendritic Spine Density ◽  
Chronic Social Defeat Stress ◽  
The Brain ◽  
Susceptible Group

ObjectiveAlthough alterations in the dendritic spine density in the brain regions may play a role in the stress-induced depression-like phenotype, the precise mechanisms are unknown. The aim was to investigate the role of spine density in the brain regions after chronic social defeat stress (CSDS).MethodsWe examined dendritic spine density in the medial prefrontal cortex (mPFC), CA1, CA3, dentate gyrus (DG) of hippocampus, nucleus accumbens (NAc), and ventral tegmental area (VTA) of susceptible and resilient mice after CSDS.ResultsSpine density in the prelimbic area of mPFC, CA3, and DG in the susceptible group, but not resilient group, was significantly lower than control group. In contrast, spine density in the NAc and VTA in the susceptible group, but not resilient group, was significantly higher than control group.ConclusionsThe results suggest that regional differences in spine density may contribute to resilience versus susceptibility in mice subjected to CSDS.

scholarly journals FMRP regulates the subcellular distribution of cortical dendritic spine density in a non-cell-autonomous manner

2021 ◽  
pp. 105253
Author(s):  
Katherine M. Bland ◽  
Adam Aharon ◽  
Eden L. Widener ◽  
M. Irene Song ◽  
Zachary O. Casey ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Subcellular Distribution ◽  
Spine Density ◽  
Dendritic Spine Density

scholarly journals BDNF-TrkB controls cocaine-induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors

2017 ◽  
Vol 114 (35) ◽  
pp. 9469-9474 ◽  
Author(s):  
Ethan M. Anderson ◽  
Anne Marie Wissman ◽  
Joyce Chemplanikal ◽  
Nicole Buzin ◽  
Daniel Guzman ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Dendritic Spine ◽  
Morphological Changes ◽  
Dominant Negative ◽  
Addictive Behaviors ◽  
Spine Density ◽  
Nucleus Accumbens Shell ◽  
Self Administration ◽  
Dendritic Spine Density ◽  
Chronic Cocaine

Chronic cocaine use is associated with prominent morphological changes in nucleus accumbens shell (NACsh) neurons, including increases in dendritic spine density along with enhanced motivation for cocaine, but a functional relationship between these morphological and behavioral phenomena has not been shown. Here we show that brain-derived neurotrophic factor (BDNF) signaling through tyrosine kinase B (TrkB) receptors in NACsh neurons is necessary for cocaine-induced dendritic spine formation by using either localized TrkB knockout or viral-mediated expression of a dominant negative, kinase-dead TrkB mutant. Interestingly, augmenting wild-type TrkB expression after chronic cocaine self-administration reverses the sustained increase in dendritic spine density, an effect mediated by TrkB signaling pathways that converge on extracellular regulated kinase. Loss of TrkB function after cocaine self-administration, however, leaves spine density intact but markedly enhances the motivation for cocaine, an effect mediated by specific loss of TrkB signaling through phospholipase Cgamma1 (PLCγ1). Conversely, overexpression of PLCγ1 both reduces the motivation for cocaine and reverses dendritic spine density, suggesting a potential target for the treatment of addiction in chronic users. Together, these findings indicate that BDNF-TrkB signaling both mediates and reverses cocaine-induced increases in dendritic spine density in NACsh neurons, and these morphological changes are entirely dissociable from changes in addictive behavior.

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