Drebrin A regulates dendritic spine plasticity and synaptic function in mature cultured hippocampal neurons

2009 ◽  
Vol 122 (4) ◽  
pp. 524-534 ◽  
Author(s):  
A. Ivanov ◽  
M. Esclapez ◽  
C. Pellegrino ◽  
T. Shirao ◽  
L. Ferhat
2013 ◽  
Vol 128 (2) ◽  
pp. 246-255 ◽  
Author(s):  
Akira Oda ◽  
Kanato Yamagata ◽  
Saya Nakagomi ◽  
Hiroshi Uejima ◽  
Pattama Wiriyasermkul ◽  
...  

2016 ◽  
Vol 27 (25) ◽  
pp. 4055-4066 ◽  
Author(s):  
Matylda Roszkowska ◽  
Anna Skupien ◽  
Tomasz Wójtowicz ◽  
Anna Konopka ◽  
Adam Gorlewicz ◽  
...  

Synaptic cell adhesion molecules regulate signal transduction, synaptic function, and plasticity. However, their role in neuronal interactions with the extracellular matrix (ECM) is not well understood. Here we report that the CD44, a transmembrane receptor for hyaluronan, modulates synaptic plasticity. High-resolution ultrastructural analysis showed that CD44 was localized at mature synapses in the adult brain. The reduced expression of CD44 affected the synaptic excitatory transmission of primary hippocampal neurons, simultaneously modifying dendritic spine shape. The frequency of miniature excitatory postsynaptic currents decreased, accompanied by dendritic spine elongation and thinning. These structural and functional alterations went along with a decrease in the number of presynaptic Bassoon puncta, together with a reduction of PSD-95 levels at dendritic spines, suggesting a reduced number of functional synapses. Lack of CD44 also abrogated spine head enlargement upon neuronal stimulation. Moreover, our results indicate that CD44 contributes to proper dendritic spine shape and function by modulating the activity of actin cytoskeleton regulators, that is, Rho GTPases (RhoA, Rac1, and Cdc42). Thus CD44 appears to be a novel molecular player regulating functional and structural plasticity of dendritic spines.


2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Chunhui Zhao ◽  
Ping Su ◽  
Cui Lv ◽  
Limin Guo ◽  
Guoqiong Cao ◽  
...  

Synaptic structural and functional damage is a typical pathological feature of Alzheimer’s disease (AD). Normal axonal mitochondrial function and transportation are vital to synaptic function and plasticity because they are necessary for maintaining cellular energy supply and regulating calcium and redox signalling as well as synaptic transmission and vesicle release. Amyloid-β (Aβ) accumulation is another pathological hallmark of AD that mediates synaptic loss and dysfunction by targeting mitochondria. Therefore, it is important to develop strategies to protect against synaptic mitochondrial damage induced by Aβ. The present study examined the beneficial effects of berberine, a natural isoquinoline alkaloid extracted from the traditional medicinal plant Coptis chinensis, on Aβ-induced mitochondrial and synaptic damage in primary cultured hippocampal neurons. We demonstrate that berberine alleviates axonal mitochondrial abnormalities by preserving the mitochondrial membrane potential and preventing decreases in ATP, increasing axonal mitochondrial density and length, and improving mitochondrial motility and trafficking in cultured hippocampal neurons. Although the underlying protective mechanism remains to be elucidated, the data suggest that the effects of berberine were in part related to its potent antioxidant activity. These findings highlight the neuroprotective and specifically mitoprotective effects of berberine treatment under conditions of Aβ enrichment.


2009 ◽  
Vol 2 (3) ◽  
pp. 268-270 ◽  
Author(s):  
Anton Ivanov ◽  
Monique Esclapez ◽  
Lotfi Ferhat

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