scholarly journals Hippocampal proteoglycans brevican and versican are linked to spatial memory of Sprague-Dawley rats in the morris water maze

2014 ◽  
Vol 130 (6) ◽  
pp. 797-804 ◽  
Author(s):  
Sivaprakasam R. Saroja ◽  
Ajinkya Sase ◽  
Susanne G. Kircher ◽  
Jia Wan ◽  
Johannes Berger ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Gastrodin attenuates lithium-pilocarpine-induced epilepsy by activating AMPK-mediated PPARα in a juvenile rat model

2021 ◽  
Author(s):  
Yanfei Yang ◽  
Yabin Li ◽  
Jinli Han ◽  
Yanfen Wang
Keyword(s):  
Morris Water Maze ◽  
Rat Model ◽  
Neurological Disease ◽  
Water Maze ◽  
Therapeutic Potential ◽  
Pediatric Epilepsy ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Electroencephalogram Eeg ◽  
Histological Staining

Abstract Gastrodin has shown the potential as an anticonvulsant. Epilepsy is a neurological disease with significant effects in children. In the current study, the therapeutic potential of gastrodin in handling pediatric epilepsy was explored by focusing on AMPK/PPARα pathway. Three-week-old Sprague-Dawley rats were subjected to lithium-pilocarpine method to induce epileptic symptoms and then administrated with gastrodin. The effects of gastrodin on rats were firstly assessed using electroencephalogram (EEG) recording, Racine classification, Morris water maze (MWM) test, and histological staining. The levels of BDNF and NGF, and the activity of AMPK/PPARα were measured. Based on the results of EEG, behavior analyses, and histological staining, epileptic symptoms were significantly alleviated by gastrodin. Moreover, the administration of gastrodin also suppressed the levels of BDNF and NGF, and activated AMPK/PPARα pathway. In conclusion, our results demonstrated that gastrodin contributed to the alleviation of pediatric epilepsy by activating AMPK/PPARα signaling transduction.

Intrahippocampal co-administration of nicotine and O-acetyl-L-carnitine prevents the H-89-induced spatial learning deficits in Morris water maze

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Mahmoud Hashemzaei ◽  
Najmeh Baratzadeh ◽  
Iraj Sharamian ◽  
Sahar Fanoudi ◽  
Mehdi Sanati ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Spatial Memory ◽  
Morris Water Maze ◽  
Spatial Learning ◽  
Water Maze ◽  
Synergistic Effects ◽  
Deionized Water ◽  
Learning Deficits ◽  
Learning Impairments ◽  
Morris Water Maze Task

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.

scholarly journals Long-term potentiation is independent of the C-tail of the GluA1 AMPA receptor subunit

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Javier Díaz-Alonso ◽  
Wade Morishita ◽  
Salvatore Incontro ◽  
Jeffrey Simms ◽  
Julia Holtzman ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Morris Water Maze ◽  
Ampa Receptor ◽  
Water Maze ◽  
Long Term Potentiation ◽  
Receptor Subunit ◽  
Terminal Domain ◽  
Term Potentiation ◽  
Ampa Receptor Subunit

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.

Haloperidol and Clozapine Reverse MK-801-Induced Deficits in Hypoactivity, but Not the Impairment of Spatial Memory in Sprague-Dawley Rats

2014 ◽  
Vol 10 (2) ◽  
pp. 120-128 ◽  
Author(s):  
Huanzhong Liu ◽  
Zhenhua Ren ◽  
Jian Zhong ◽  
Han Cai ◽  
Xuequan Chen ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Sprague Dawley ◽  
Mk 801 ◽  
Sprague Dawley Rats

Edible Salt Plus D-Gal Accelerate Aging Progress

2014 ◽  
Vol 955-959 ◽  
pp. 326-334 ◽  
Author(s):  
Peng Wan ◽  
Cheng Xi Wei ◽  
Jian Long Wu ◽  
Qing Hua Jin
Keyword(s):  
Protein Expression ◽  
Spatial Memory ◽  
Morris Water Maze ◽  
Water Maze ◽  
Molecular Mechanisms ◽  
Potential Role ◽  
Memory Function ◽  
Accelerate Aging ◽  
Cox 2

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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