Intrahippocampal Injections of Ghrelin and Aerobic Physical Exercise: Effects on Learning and Passive Avoidance Memory in Rats

2021 ◽  
Author(s):  
M. Farzin ◽  
P. Babaei ◽  
M. Rostampour
Keyword(s):  
Physical Exercise ◽  
Passive Avoidance ◽  
Avoidance Memory

scholarly journals The Protective Effect of Celecoxib on CA1 Hippocampal Neurons and Oxidative Stress in a Rat Model of Parkinson’s Disease

2019 ◽  
Author(s):  
Maryam Sarbishegi ◽  
Hamidreza Mahmoudzadeh-sagheb ◽  
Zahra Heidari ◽  
Farzaneh Baharvand
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protective Effect ◽  
Passive Avoidance ◽  
Rat Model ◽  
Hippocampal Neurons ◽  
Wistar Rat ◽  
Tunel Staining ◽  
Model Animal ◽  
Avoidance Memory

Abstract- Several studies point to an important role of neuroinflammation in Parkinson's disease (PD). Cognitive and memory impairments have been known in the early stages of PD. In the present study, we examined the effects of celecoxib (CLX), a selective inhibitor of cyclooxygenase-2 (COX-2), on hippocampus cell loss, passive avoidance memory and antioxidant status in a rat model of PD. We used the subcutaneous injection of 2.5 mg/kg/48h rotenone (ROT) for 4 weeks for induction of PD in a male Wistar rat. Animals were randomized to 4 groups (n=12): Control, sham, PD and PD+CLX group that receive celecoxib (20 mg/kg/day) for 4 weeks. Passive avoidance memory evaluated. We also determined the protective effect of CLX on a number of CA1 neurons in Nissl and TUNEL staining. Total antioxidant capacity (TAC) and malondialdehyde (MDA) a marker of lipid peroxidation in hippocampus assessed. Our findings indicated administration of CLX increase the passive avoidance memory (P<0.05), and by a decrease in apoptosis caused an increase in viable pyramidal neurons in CA1 hippocampus (P<0.01). On the other hand, CLX markedly reduced MDA level and increased TAC in the hippocampus of the PD model animal (P<0.05). It seems CLX with anti-inflammatory and antiapoptotic effect could prevent neurons loss and memory impairment which induced in PD.

Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice

2015 ◽  
Vol 169 (1) ◽  
pp. 106-113 ◽  
Author(s):  
Kaveh Tabrizian ◽  
Abdolmajid Yazdani ◽  
Behnam Baheri ◽  
Borna Payandemehr ◽  
Mehdi Sanati ◽  
...  
Keyword(s):  
Passive Avoidance ◽  
Zinc Chloride ◽  
Lead Acetate ◽  
Memory Retention ◽  
Avoidance Memory

scholarly journals Correction to Furoxans (Oxadiazole-N-oxides) with Attenuated Reactivity Are Neuroprotective, Cross the Blood Brain Barrier, and Improve Passive Avoidance Memory

2018 ◽  
Vol 61 (13) ◽  
pp. 5773-5773
Author(s):  
Austin Horton ◽  
Kevin Nash ◽  
Ethel Tackie-Yarboi ◽  
Alexander Kostrevski ◽  
Adam Novak ◽  
...  
Keyword(s):  
Passive Avoidance ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain ◽  
Avoidance Memory

scholarly journals Apolipoprotein E Antibodies Affect the Retention of Passive Avoidance Memory in the Chick

1998 ◽  
Vol 6 (3) ◽  
pp. 29-40 ◽  
Author(s):  
Chris Lancashire ◽  
Radmila Mileusnic ◽  
Steven P.R. Rose
Keyword(s):  
Risk Factors ◽  
Apolipoprotein E ◽  
Passive Avoidance ◽  
Residence Time ◽  
Memory Formation ◽  
Avoidance Task ◽  
Brain Distribution ◽  
The Brain ◽  
Avoidance Memory

Isoforms of apolipoprotein E (ApoE) have been implicated as risk factors in Alzheimer’s disease. We have, therefore, examined the possible role of ApoE in memory formation, using a one-trial passive avoidance task in day-old chicks. Birds were trained on the task and then at various times pre or post-training were injected intracerebrally with anti-ApoE. Immunofluorescence staining demonstrated the presence of the antibody bound to the neuropil, close to the injection site and adjacent to the ventricle, with a residence time in the brain of up to 30 min. Chicks that were injected 30 min pre-training or just post-training with 5μg/ hemisphere of the antibody learned the task, but were amnesic when tested at 30 min or at subsequent times up to 24 hr Post-training. When tested at 24 hr, birds injected 5.5 hr post-training showed unimpaired retention. Birds injected with 5μg/hemisphere of anti-ApoA-I (which has a brain distribution similar to that of anti-ApoE) at 30 min pretraining showed no amnesia, indicating the specificity of the effect to the ApoE. Possible mechanisms for this effect are discussed.

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