scholarly journals An in vitro reproduction of stress-induced memory defects: Effects of corticoids on dendritic spine dynamics

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Shinichi Saito ◽  
Satoshi Kimura ◽  
Naoki Adachi ◽  
Tadahiro Numakawa ◽  
Akihiko Ogura ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Spine Dynamics

The effect of kainic acid on hippocampal dendritic spine dynamics

2016 ◽  
Vol 26 ◽  
pp. S302
Author(s):  
T. Lortkipanidze ◽  
T. Bikashvili ◽  
M. Kiladze
Keyword(s):  
Kainic Acid ◽  
Dendritic Spine ◽  
Spine Dynamics

scholarly journals Interaction of Ankycorbin and Tara regulates dendritic spine dynamics

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S344
Author(s):  
Soo Jeong Kim ◽  
Youngsik Woo ◽  
Su-Jin Noh ◽  
Yubin Won ◽  
Eun Byul Cho ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Spine Dynamics

scholarly journals Bergmann glial ensheathment of dendritic spines regulates synapse number without affecting spine motility

2010 ◽  
Vol 6 (3) ◽  
pp. 193-200 ◽  
Author(s):  
Jocelyn J. Lippman Bell ◽  
Tamar Lordkipanidze ◽  
Natalie Cobb ◽  
Anna Dunaevsky
Keyword(s):  
Purkinje Cell ◽  
Dendritic Spines ◽  
Dendritic Spine ◽  
Adenoviral Vector ◽  
Spine Density ◽  
Dendritic Spine Density ◽  
Spine Dynamics

In the cerebellum, lamellar Bergmann glial (BG) appendages wrap tightly around almost every Purkinje cell dendritic spine. The function of this glial ensheathment of spines is not entirely understood. The development of ensheathment begins near the onset of synaptogenesis, when motility of both BG processes and dendritic spines are high. By the end of the synaptogenic period, ensheathment is complete and motility of the BG processes decreases, correlating with the decreased motility of dendritic spines. We therefore have hypothesized that ensheathment is intimately involved in capping synaptogenesis, possibly by stabilizing synapses. To test this hypothesis, we misexpressed GluR2 in an adenoviral vector in BG towards the end of the synaptogenic period, rendering the BG α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) Ca2+-impermeable and causing glial sheath retraction. We then measured the resulting spine motility, spine density and synapse number. Although we found that decreasing ensheathment at this time does not alter spine motility, we did find a significant increase in both synaptic pucta and dendritic spine density. These results indicate that consistent spine coverage by BG in the cerebellum is not necessary for stabilization of spine dynamics, but is very important in the regulation of synapse number.

scholarly journals Actinin-4 Governs Dendritic Spine Dynamics and Promotes Their Remodeling by Metabotropic Glutamate Receptors

2015 ◽  
Vol 290 (26) ◽  
pp. 15909-15920 ◽  
Author(s):  
Magdalena Kalinowska ◽  
Andrés E. Chávez ◽  
Stefano Lutzu ◽  
Pablo E. Castillo ◽  
Feliksas F. Bukauskas ◽  
...  
Keyword(s):  
Glutamate Receptors ◽  
Dendritic Spine ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate ◽  
Spine Dynamics

scholarly journals Drug-Paired Contextual Stimuli Increase Dendritic Spine Dynamics in Select Nucleus Accumbens Neurons

2016 ◽  
Vol 41 (8) ◽  
pp. 2178-2187 ◽  
Author(s):  
Bryan F Singer ◽  
Nancy Bubula ◽  
Dongdong Li ◽  
Magdalena M Przybycien-Szymanska ◽  
Vytautas P Bindokas ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Dendritic Spine ◽  
Contextual Stimuli ◽  
Spine Dynamics

Experience-dependent dendritic spine dynamics in the mouse cortex

2009 ◽  
Vol 65 ◽  
pp. S7 ◽  
Author(s):  
Wen-Biao Gan ◽  
Guang Yang ◽  
Feng Pan
Keyword(s):  
Dendritic Spine ◽  
Mouse Cortex ◽  
Spine Dynamics

scholarly journals Transcriptome profiling of the ventral pallidum reveals a role for pallido-thalamic neurons in cocaine reward

2021 ◽  
Author(s):  
Michel Engeln ◽  
Megan E Fox ◽  
Ramesh Chandra ◽  
Eric Y Choi ◽  
Hyungwoo Nam ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Drug Use ◽  
Dendritic Spine ◽  
Transcriptome Profiling ◽  
Ventral Pallidum ◽  
Projection Neurons ◽  
Specific Gene ◽  
Thalamic Neurons ◽  
Spine Dynamics

Psychostimulant exposure alters the activity of ventral pallidum (VP) projection-neurons. However, the molecular underpinnings of these circuit dysfunctions are unclear. Using RNA-sequencing followed by circuit-specific gene expression assays, we revealed a key role for the VP to mediodorsal thalamus (VP-MDT) projection neurons in cocaine-related behaviors in mice. Our analyses demonstrated that the transcription factor Nr4a1 bidirectionally modulated dendritic spine dynamics in VP-MDT neurons and positively regulated pathological drug use.

scholarly journals The Polyadenosine RNA Binding Protein ZC3H14 is Required in Mice for Proper Dendritic Spine Density

2020 ◽  
Author(s):  
Stephanie K. Jones ◽  
Jennifer Rha ◽  
Sarah Kim ◽  
Kevin J. Morris ◽  
Omotola F. Omotade ◽  
...  
Keyword(s):  
Dendritic Spine ◽  
Hippocampal Neurons ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Spine Density ◽  
Dendritic Spine Density

AbstractZC3H14 (Zinc finger CysCysCysHis domain-containing protein 14), an evolutionarily conserved member of a class of tandem zinc finger (CCCH) polyadenosine (polyA) RNA binding proteins, is associated with a form of heritable, nonsyndromic autosomal recessive intellectual disability. Previous studies of a loss of function mouse model, Zc3h14Δex13/Δex13, provide evidence that ZC3H14 is essential for proper brain function, specifically for working memory. To expand on these findings, we analyzed the dendrites and dendritic spines of hippocampal neurons from Zc3h14Δex13/Δex13 mice, both in situ and in vitro. These studies reveal that loss of ZC3H14 is associated with a decrease in total spine density in hippocampal neurons in vitro as well as in the dentate gyrus of 5-month old mice analyzed in situ. This reduction in spine density in vitro results from a decrease in the number of mushroom-shaped spines, which is rescued by exogenous expression of ZC3H14. We next performed biochemical analyses of synaptosomes prepared from whole wild-type and Zc3h14Δex13/Δex13 mouse brains to determine if there are changes in steady state levels of postsynaptic proteins upon loss of ZC3H14. We found that ZC3H14 is present within synaptosomes and that a crucial postsynaptic protein, CaMKIIα, is significantly increased in these synaptosomal fractions upon loss of ZC3H14. Together, these results demonstrate that ZC3H14 is necessary for proper dendritic spine density in cultured hippocampal neurons and in some regions of the mouse brain. These findings provide insight into how a ubiquitously expressed RNA binding protein leads to neuronal-specific defects that result in brain dysfunction.

scholarly journals Unique axon-to-soma signaling pathways mediate dendritic spine loss and hyper-excitability post-axotomy

2019 ◽  
Author(s):  
Tharkika Nagendran ◽  
Anne Marion Taylor
Keyword(s):  
Dendritic Spine ◽  
Calcium Release ◽  
Pyramidal Neurons ◽  
Axon Regeneration ◽  
Sodium Influx ◽  
Axon Injury ◽  
Synapse Loss ◽  
Sodium Calcium ◽  
Axon Damage

AbstractAxon damage may cause axon regeneration, retrograde synapse loss, and hyper-excitability, all of which affect recovery following acquired brain injury. While axon regeneration is studied extensively, less is known about signaling mediating retrograde synapse loss and hyper-excitability, especially in long projection pyramidal neurons. To investigate intrinsic injury signaling within neurons, we use an in vitro microfluidic platform that models dendritic spine loss and delayed hyper-excitability following remote axon injury. Our data show that sodium influx and reversal of sodium calcium exchangers (NCXs) at the site of axotomy, mediate dendritic spine loss following axotomy. In contrast, sodium influx and NCX reversal alone are insufficient to cause retrograde hyper-excitability. We found that calcium release from axonal ER is critical for the induction of hyper-excitability and inhibition loss. These data suggest that synapse loss and hyper-excitability are uncoupled responses following axon injury. Further, axonal ER may play a critical and underappreciated role in mediating retrograde hyper-excitability within the CNS.

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