scholarly journals Antibodies to Glutamate Facilitate Spatial Memory Formation in the Morris Water Maze in Aging C57BL/6 mice

2020 ◽  
Vol 169 (1) ◽  
pp. 5-8
Author(s):  
T. V. Davydova ◽  
M. A. Gruden ◽  
V. S. Kudrin ◽  
V. B. Narkevich ◽  
L. A. Vetrile ◽  
...  
NeuroImage ◽  
2019 ◽  
Vol 202 ◽  
pp. 116069 ◽  
Author(s):  
Nadjalisse C. Reynolds ◽  
Jimmy Y. Zhong ◽  
Cherita A. Clendinen ◽  
Scott D. Moffat ◽  
Kathy R. Magnusson

Author(s):  
Mahmoud Hashemzaei ◽  
Najmeh Baratzadeh ◽  
Iraj Sharamian ◽  
Sahar Fanoudi ◽  
Mehdi Sanati ◽  
...  

Abstract Objectives H-89 (a protein kinase AII [PKA II] inhibitor) impairs the spatial memory in the Morris water maze task in rats. In the present study, we aimed to study the protective effects of nicotine and O-acetyl-L-carnitine against H-89-induced spatial memory deficits. Methods Spatial memory impairment was induced by the bilateral intrahippocampal administration of 10 µM H-89 (dissolved in dimethyl sulfoxide, DMSO) to rats. The rats then received bilateral administrations of either nicotine (1 μg/μL, dissolved in saline) or O-acetyl-L-carnitine (100 μM/side, dissolved in deionized water) alone and in combination. Control groups received either saline, deionized water, or DMSO. Results The H-89-treated animals showed significant increases in the time and distance travelled to find hidden platforms, and there was also a significant decrease in the time spent in the target quadrant compared to DMSO-treated animals. Nicotine and O-acetyl-L-carnitine had no significant effects on H-89-induced spatial learning impairments alone, but the bilateral intrahippocampal co-administration of nicotine and O-acetyl-L-carnitine prevented H-89-induced spatial learning deficits and increased the time spent in the target quadrant in comparison with H-89-treated animals. Conclusions Our results indicated the potential synergistic effects of nicotine and O-acetyl-L-carnitine in preventing protein kinase AII inhibitor (H-89)-induced spatial learning impairments.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Javier Díaz-Alonso ◽  
Wade Morishita ◽  
Salvatore Incontro ◽  
Jeffrey Simms ◽  
Julia Holtzman ◽  
...  

We tested the proposal that the C-terminal domain (CTD) of the AMPAR subunit GluA1 is required for LTP. We found that a knock-in mouse lacking the CTD of GluA1 expresses normal LTP and spatial memory, assayed by the Morris water maze. Our results support a model in which LTP generates synaptic slots, which capture passively diffusing AMPARs.


2014 ◽  
Vol 955-959 ◽  
pp. 326-334 ◽  
Author(s):  
Peng Wan ◽  
Cheng Xi Wei ◽  
Jian Long Wu ◽  
Qing Hua Jin

Edible salt (ES) is also thought to exacerbate the symptoms of Alzheimer, however, the in vivo function of ES remains poorly understand. In this work, we investigated the phenomenon using the model of Alzheimer induced by D-gal. The behavious examination results exhibited that D-gal plus ES can weaken spatial memory function in the Morris water maze; the activities of T-SOD, GSH-Px and the CAT level in both hippocampus and cortex showed that D-gal plus ES decreased the expression of T-SOD and GSH-Px, but the expression of CAT increased, the protein expression determined in both of the hippocampus and cortex demonstrated that COX-2, iNOS, NFκ-B-p65-N proteins were significantly increased. It is possible that ES acts through several mechanisms, mediating a potential role in memory damage in mice. These results suggest that further study is necessary to evaluate the effect of salt on damage of memory and to determine the molecular mechanisms.


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