avoidance memory
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2022 ◽  
Vol 8 (1) ◽  
pp. 7-16
Author(s):  
Adeleh Jafari ◽  
◽  
Parvin Babaei ◽  
Kambiz Rohampour ◽  
Samira Rashtiani ◽  
...  

Background: Numerous pieces of evidence support that oxidative stress is a key factor in the pathogenesis of neurodegenerative diseases, like Alzheimer’s Disease (AD). Suppression of oxidative stress is an attractive strategy and flavonoids as potent natural antioxidants are extremely noticeable. Objectives: In this study, the effects of Kaempferol (KMP) were evaluated on passive avoidance memory, hippocampal Nrf-2, and beclin-1 expression in a rat model of Aβ1-42 –induced AD. Materials & Methods: Forty male Wistar rats weighing 200-250 g were divided into five groups (n=8); sham-operated, AD model, and KMP treatment (5, 7.5, 10 mg/kg, i.p. for three weeks). Animals received an intracerebroventricular injection of amyloid-beta (1-42) to establish an AD model. Passive avoidance memory of rats was evaluated using a shuttle box on day 21; Step-Through Latency (STL) and time spent in The Dark Compartment (TDC) were recorded. Then, hippocampus homogenates were used for biochemical and molecular analysis by real-time PCR, western blot, and ELISA. Results: It was found that KMP improved memory evidenced by increased STL (P≤0.05) and decreased TDC (p≤0.01). KMP also increased the levels of Total Antioxidant Capacity (TAC) in the hippocampus of rats (P≤0.05). In addition, KMP enhanced the expression of Nrf-2 mRNA (P≤0.001) and beclin-1 protein in the hippocampus tissues (P≤0.001). Conclusion: Overall, it is suggested that the memory-improving effect of KMP is mediated, at least in part, by enhancing Nrf-2 and TAC. KMP is also able to induce autophagy through the expression of beclin-1.


2021 ◽  
Vol 10 ◽  
pp. e2254
Author(s):  
Samira Malekzadeh ◽  
Mohammad Amin Edalatmanesh ◽  
Davood Mehrabani ◽  
Mehrdad Shariati

Background: According to the increasing incidence of Alzheimer’s disease (AD), this study aimed to investigate the effect of dental pulp stem cells (DPSCs) transplantation on passive avoidance memory and neuroinflammation in trimethyltin (TMT)-induced AD rat model. Materials and Methods: In this experimental study, 18 male Wistar rats were randomly divided into three groups: the control that rats received 8 mg/kg TMT plus 0.5 ml phosphate buffered saline (PBS) and TMT+DPSCs (TMT + 1×106 cells/ml DPSC in 0.5 ml PBS) groups. Then, after one month, passive avoidance test was performed. Also measured the Nuclear Factor Kappa-β (NF-Kβ) serum level and the percentage of damaged neurons in the hippocampus were determined. Results: DPSCs transplantation showed significantly increased step-through latency to the dark compartment in comparison with control and TMT+PBS groups in 24 hours after shock. Also, time spent in the dark compartment of TMT+DPSCs significantly decreased compared to control and TMT+PBS groups in 24 and 48 hours after shock (P<0.05). Furthermore, DPSCs transplantation significantly decreased the NF-Kβ serum level and percentage of damaged pyramidal neurons of CA1 compared with TMT+PBS (P<0.05). Conclusion: DPSCs transplantation improved memory and learning, regulated NF-Kβ serum level, and decreased damage neurons of CA1 hippocampus in TMT-induced AD rat model.


2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Vahid Reza Ostovan ◽  
Zeynab Amiri ◽  
Leila Moezi ◽  
Fatema Pirsalami ◽  
Zahra Esmaili ◽  
...  

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Andressa Radiske ◽  
Maria Carolina Gonzalez ◽  
Janine I. Rossato ◽  
Gênedy Apolinário ◽  
João R. de Oliveira ◽  
...  

AbstractAvoidance memory is destabilized when recalled concurrently with conflicting information, and must undergo a hippocampus-dependent restabilization process called reconsolidation to persist. CaMKII is a serine/threonine protein kinase essential for memory processing; however, its possible involvement in avoidance memory reconsolidation has not yet been studied. Using pharmacological, electrophysiological and optogenetic tools, we found that in adult male Wistar rats hippocampal CaMKII is necessary to reconsolidate avoidance memory, but not to keep it stored while inactive, and that blocking reconsolidation via CaMKII inhibition erases learned avoidance responses.


2021 ◽  
pp. 113313
Author(s):  
Mitra Khakpoor ◽  
Salar Vaseghi ◽  
Mohammad-Hossein Mohammadi-Mahdiabadi-Hasani ◽  
Mohammad Nasehi

2021 ◽  
Vol 15 (2) ◽  
pp. 99-108
Author(s):  
Sheyda Najafi ◽  
◽  
Mahmoud Hashemzaei ◽  
Maryam Sadeghi ◽  
Sajedeh Seyed Mousavi ◽  
...  

Background: The toxic effect of sodium arsenate on nervous system has been shown; but the protective effects of several compounds against sodium arsenate are not clear. This study aimed to investigate the protective effects of nicotine and bucladesine, two positive modulators of neuronal function, on sodium arsenate toxicity against avoidance memory impairment. Methods: Male mice (N=154) were assigned to 22 groups (12 experimental and 10 control) of seven animals each and were treated as follows: sodium arsenate (2.5, 5, or 10 mg/kg) for 28 days, nicotine (1 mg/kg) for either 1, 2, or 4 days, bucladesine (600 nM/mouse) for either 1, 2, or 4 days, and nicotine (1 mg/kg)+bucladesine (600 nM/mouse)+sodium arsenate (2.5 mg/kg). The last group was treated with 2.5 mg/kg sodium arsenate first, and then received the combination of nicotine and bucladesine for 1, 2, or 4-days. The corresponding control groups did not receive any drug but either saline, deionized water, or combination of deionized water and DMSO, but went through the same procedure as other animals. All mice were trained 24 h in the step-through passive avoidance task. The avoidance memory retention was assessed at 24, 48, 96, and 168 h after the training period by measuring the time they stayed in a dark chamber. Results: All sodium arsenate doses significantly reduced the time stayed in the dark chamber regardless of the treatment duration (24, 48, 96 & 168 h) after training. Both nicotine and bucladesine, whether used singly or combined for 1, 2, and 4 days significantly enhanced the time latency compared to the controls at all of the experimental timepoints following the training. Conclusion: Nicotine and bucladesine showed synergistic effects and reversed the sodium arsenate-induced avoidance memory deficits in mice.


2021 ◽  
Vol 26 (1) ◽  
pp. 67-74
Author(s):  
Mahmoud Hashemzaei ◽  
Sahar Fanoudi ◽  
Mohadeseh Najari ◽  
Mansoureh Fotouhi ◽  
Maryam Belaran ◽  
...  

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