Conditional self-discrimination enhances dendritic spine number and dendritic length at prefrontal cortex and hippocampal neurons of rats

Synapse ◽  
2015 ◽  
Vol 69 (11) ◽  
pp. 543-552 ◽  
Author(s):  
Julio C. Penagos-Corzo ◽  
Andrea Bonilla ◽  
Antonio Rodríguez-Moreno ◽  
Gonzalo Flores ◽  
José V. Negrete-Díaz
Synapse ◽  
2010 ◽  
pp. NA-NA ◽  
Author(s):  
Faviola Alcantara-Gonzalez ◽  
Ismael Juarez ◽  
Oscar Solis ◽  
Isaura Martinez-Tellez ◽  
Israel Camacho-Abrego ◽  
...  

2018 ◽  
Vol 19 (8) ◽  
pp. 2323 ◽  
Author(s):  
Yu-Chia Kao ◽  
I-Fang Wang ◽  
Kuen-Jer Tsai

Microribonucleic acids (miRNAs) play a pivotal role in numerous aspects of the nervous system and are increasingly recognized as key regulators in neurodegenerative diseases. This study hypothesized that miR-34c, a miRNA expressed in mammalian hippocampi whose expression level can alter the hippocampal dendritic spine density, could induce memory impairment akin to that of patients with Alzheimer’s disease (AD) in mice. In this study, we showed that miR-34c overexpression in hippocampal neurons negatively regulated dendritic length and spine density. Hippocampal neurons transfected with miR-34c had shorter dendrites on average and fewer filopodia and spines than those not transfected with miR-34c (control mice). Because dendrites and synapses are key sites for signal transduction and fundamental structures for memory formation and storage, disrupted dendrites can contribute to AD. Therefore, we supposed that miR-34c, through its effects on dendritic spine density, influences synaptic plasticity and plays a key role in AD pathogenesis.


2021 ◽  
Vol 896 ◽  
pp. 173883
Author(s):  
Néstor I. Martínez-Torres ◽  
Nallely Vázquez-Hernández ◽  
Fabiola L. Martín-Amaya-Barajas ◽  
Mario Flores-Soto ◽  
Ignacio González-Burgos

2021 ◽  
Vol 179 ◽  
pp. 107409
Author(s):  
M.L. Perea Vega ◽  
M.S. Sanchez ◽  
G. Fernández ◽  
M.G. Paglini ◽  
M. Martin ◽  
...  

2019 ◽  
Vol 80 ◽  
pp. 889-899 ◽  
Author(s):  
Kristie Leigh Smith ◽  
Mustafa S. Kassem ◽  
David J. Clarke ◽  
Michael P. Kuligowski ◽  
Miguel A. Bedoya-Pérez ◽  
...  

2020 ◽  
Vol 55 (4) ◽  
pp. 357-366
Author(s):  
Wenyang Jin ◽  
Mizhu Sun ◽  
Bingbing Yuan ◽  
Runzhi Wang ◽  
Hongtao Yan ◽  
...  

Abstract Aims Ethanol is a small molecule capable of interacting with numerous targets in the brain, the mechanisms of which are complex and still poorly understood. Studies have revealed that ethanol-induced hippocampal neuronal injury is associated with oxidative stress. Grape seed procyanidin (GSP) is a new type of antioxidant that is believed to scavenge free radicals and be anti-inflammatory. This study evaluated the ability and mechanism by which the GSP improves ethanol-induced hippocampal neuronal injury. Methods Primary cultures of hippocampal neurons were exposed to ethanol (11, 33 and 66 mM, 1, 4, 8, 12 and 24 h) and the neuroprotective effects of GSP were assessed by evaluating the activity of superoxide dismutase (SOD), the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) and cell morphology. Results Our results indicated that GSP prevented ethanol-induced neuronal injury by reducing the levels of MDA and LDH, while increasing the activity of SOD. In addition, GSP increased the number of primary dendrites and total dendritic length per cell. Conclusion Together with previous findings, these results lend further support to the significance of developing GSP as a therapeutic tool for use in the treatment of alcohol use disorders.


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