scholarly journals Reelin supplementation enhances cognitive ability, synaptic plasticity, and dendritic spine density

2011 ◽  
Vol 18 (9) ◽  
pp. 558-564 ◽  
Author(s):  
J. T. Rogers ◽  
I. Rusiana ◽  
J. Trotter ◽  
L. Zhao ◽  
E. Donaldson ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Cognitive Ability ◽  
Dendritic Spine ◽  
Spine Density ◽  
Dendritic Spine Density

Rapid Effects of Estradiol on Dendritic Spines and Synaptic Plasticity in the Male and Female Hippocampus

2020 ◽  
pp. 38-47
Author(s):  
Asami Kato ◽  
Gen Murakami ◽  
Yasushi Hojo ◽  
Sigeo Horie ◽  
Suguru Kawato
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spine ◽  
Hippocampal Neurons ◽  
Molecular Mechanisms ◽  
Hippocampal Slices ◽  
Spine Density ◽  
Male And Female ◽  
Dendritic Spine Density ◽  
Male And Female Rats ◽  
Rapid Modulation

Although the potent estrogen, 17β‎-estradiol (E2), has long been known to regulate the hippocampal dendritic spine density and synaptic plasticity, the molecular mechanisms through which it does so are less well understood. This chapter discusses the rapid modulation of hippocampal dendritic spine density and synaptic plasticity in male and female rats, with particular attention to studies in hippocampal slices from male rats. Among the mechanisms described are the roles of specific cell-signaling kinases and estrogen receptors in mediating the effects of E2 and progesterone on hippocampal neurons. In addition, dynamic changes of spine structures over time and sex differences in spine regulation are also considered. Finally, the chapter ends by discussing the importance of local hippocampal synthesis of E2 and androgens to hippocampal spine morphology and plasticity.

scholarly journals Eps8 controls dendritic spine density and synaptic plasticity through its actin-capping activity

2013 ◽  
Vol 32 (12) ◽  
pp. 1730-1744 ◽  
Author(s):  
Elisabetta Menna ◽  
Stefania Zambetti ◽  
Raffaella Morini ◽  
Andrea Donzelli ◽  
Andrea Disanza ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spine ◽  
Spine Density ◽  
Dendritic Spine Density ◽  
Actin Capping

scholarly journals Systemic or Forebrain Neuron-Specific Deficiency of Geranylgeranyltransferase-1 Impairs Synaptic Plasticity and Reduces Dendritic Spine Density

Neuroscience ◽  
2018 ◽  
Vol 373 ◽  
pp. 207-217 ◽  
Author(s):  
David Hottman ◽  
Shaowu Cheng ◽  
Andrea Gram ◽  
Kyle LeBlanc ◽  
Li-Lian Yuan ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spine ◽  
Spine Density ◽  
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.

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