scholarly journals Early Life Sleep Disruption Alters Dendritic Spine Density and Morphology in Prairie Voles

2018 ◽  
Author(s):  
Alex Chau
Keyword(s):  
Dendritic Spine ◽  
Early Life ◽  
Sleep Disruption ◽  
Spine Density ◽  
Prairie Voles ◽  
Dendritic Spine Density

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.

Dendritic Spine Density of Pyramidal Neurons in Field CA1 of the Hippocampus Decreases due to Chronic Tryptophan Restriction

1998 ◽  
Vol 1 (3) ◽  
pp. 237-242 ◽  
Author(s):  
M.I. Pérez-Vega ◽  
G. Barajas-López ◽  
A.R. del Angel-Meza ◽  
I. González-Burgos ◽  
A. Feria-Velasco
Keyword(s):  
Dendritic Spine ◽  
Pyramidal Neurons ◽  
Spine Density ◽  
Dendritic Spine Density ◽  
Field Ca1

scholarly journals BA11 FKBP5 expression levels correlate with dendritic spine density in postmortem PTSD and controls

2015 ◽  
Vol 2 ◽  
pp. 67-72 ◽  
Author(s):  
Keith A. Young ◽  
Peter M. Thompson ◽  
Dianne A. Cruz ◽  
Douglas E. Williamson ◽  
Lynn D. Selemon
Keyword(s):  
Dendritic Spine ◽  
Spine Density ◽  
Expression Levels ◽  
Dendritic Spine Density
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