scholarly journals Comparing the Therapeutic Effects of Crocin, Escitalopram and Co-Administration of Escitalopram and Crocin on Learning and Memory in Rats with Stress-Induced Depression

2021 ◽  
Vol 28 (4) ◽  
pp. 50-62
Author(s):  
Mehran Joodaki ◽  
Maryam Radahmadi ◽  
Hojjatallah Alaei
Keyword(s):  
Learning And Memory ◽  
Recovery Period ◽  
Memory Deficits ◽  
Therapeutic Effects ◽  
Memory Impairments ◽  
Brain Functions ◽  
Depression Group ◽  
Dark Room ◽  
Control Sham ◽  
Better Than

Background: Depression affects various brain functions. According to previous studies, escitalopram influences brain functions in depression and crocin reduces memory impairments. Therefore, this study aimed to compare the therapeutic effects of using crocin and escitalopram (separately and in combination) on learning and memory in rats with stress-induced depression. Methods: Fifty-six rats were allocated into seven groups of control, sham, continuous depression, recovery period, daily injections of escitalopram, crocin and escitalopram-crocin during 14 days after inducing depression by stress. Passive avoidance (PA) test was used to assess brain functions. Results: Latency has significant differences in depression group. Also, it significantly increased in depression-crocin, depression-escitalopram and depression-escitalopram-crocin groups compared to the depression group. The dark stay (DS) time was significantly higher in the depression and depression-recovery groups. However, the DS time significantly decreased in the depression-crocin, depression-escitalopram and depression-escitalopram-crocin groups. Furthermore, the number of entrances to the dark room was significantly lower in depression-crocin and depression-escitalopram-crocin groups compared to the depression one. Conclusion: Different depression treatments (i.e. crocin, escitalopram and crocin- escitalopram) reduced depression-induced memory deficits. Crocin and escitalopram-crocin, respectively, improved brain functions and locomotor activity more than escitalopram. Comparatively, in subjects with depression, crocin, which is an effective saffron constituent, partially affected the memory deficits better than escitalopram (as a chemical component).

scholarly journals Elaeagnus glabra f. oxyphylla Attenuates Scopolamine-Induced Learning and Memory Impairments in Mice by Improving Cholinergic Transmission via Activation of CREB/NGF Signaling

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1205 ◽  
Author(s):  
Eunjin Sohn ◽  
Hye-Sun Lim ◽  
Yu Jin Kim ◽  
Bu-Yeo Kim ◽  
Joo-Hwan Kim ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Ethanol Extract ◽  
Treated Group ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Tunel Staining ◽  
Therapeutic Effects ◽  
Memory Impairments ◽  
Group A ◽  
Ngf Signaling

We aimed to investigate the therapeutic effects of an Elaeagnus glabra f. oxyphylla (EGFO) ethanol extract in mice with scopolamine-induced memory dysfunction. Fifty male mice were randomly divided into a normal control group, a scopolamine-treated group, a scopolamine and EGFO extract-treated group, and a scopolamine and tacrine-treated group. EGFO (50 or 100 mg/kg/day) was received for 21 days. Step-through passive avoidance and Y-maze tests were performed to examine the effects of treatment on learning and memory impairments. Acetylcholine (Ach) levels and acetylcholinesterase (AchE) activity were measured via an enzyme-linked immunosorbent assay (ELISA). Levels of choline acetyltransferase (ChAT), nerve growth factor (NGF), cAMP response element-binding protein (CREB), and apoptosis-related protein expression were determined via Western blot analysis. EGFO pretreatment significantly attenuated scopolamine-induced memory impairments, relative to findings observed in the scopolamine-treated group. Levels of cholinergic factors in the brain tissues were markedly attenuated in the scopolamine-treated group. EGFO treatment also attenuated neural apoptosis in scopolamine-treated mice by decreasing the expression of apoptosis-related proteins such as Bax, Bcl2, cleaved caspase-3, and TUNEL staining. These results suggest that EGFO improves memory and cognition in a mouse model of memory impairment by restoring cholinergic and anti-apoptotic activity, possibly via activation of CREB/NGF signaling.

scholarly journals Abrogation of atypical neurogenesis and vascular-derived EphA4 prevents repeated mild TBI-induced learning and memory impairments

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Kisha Greer ◽  
Erwin Kristobal Gudenschwager Basso ◽  
Colin Kelly ◽  
Alison Cash ◽  
Elizabeth Kowalski ◽  
...  
Keyword(s):  
Brain Injury ◽  
Learning And Memory ◽  
Cell Fate ◽  
Neural Progenitor Cells ◽  
Memory Deficits ◽  
Spatial Learning And Memory ◽  
Barnes Maze ◽  
Wild Type ◽  
Memory Impairments ◽  
Cell Changes

Abstract Brain injury resulting from repeated mild traumatic insult is associated with cognitive dysfunction and other chronic co-morbidities. The current study tested the effects of aberrant neurogenesis in a mouse model of repeated mild traumatic brain injury (rmTBI). Using Barnes Maze analysis, we found a significant reduction in spatial learning and memory at 24 days post-rmTBI compared to repeated sham (rSham) injury. Cell fate analysis showed a greater number of BrdU-labeled cells which co-expressed Prox-1 in the DG of rmTBI-injured mice which coincided with enhanced cFos expression for neuronal activity. We then selectively ablated dividing neural progenitor cells using a 7-day continuous infusion of Ara-C prior to rSham or rmTBI. This resulted in attenuation of cFos and BrdU-labeled cell changes and prevented associated learning and memory deficits. We further showed this phenotype was ameliorated in EphA4f./f/Tie2-Cre knockout compared to EphA4f./f wild type mice, which coincided with altered mRNA transcript levels of MCP-1, Cx43 and TGFβ. These findings demonstrate that cognitive decline is associated with an increased presence of immature neurons and gene expression changes in the DG following rmTBI. Our data also suggests that vascular EphA4-mediated neurogenic remodeling adversely affects learning and memory behavior in response to repeated insult.

scholarly journals Involvement of Cholinergic Dysfunction and Oxidative Damage in the Effects of Simulated Weightlessness on Learning and Memory in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Yongliang Zhang ◽  
Qiong Wang ◽  
Hailong Chen ◽  
Xinmin Liu ◽  
Ke Lv ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Learning And Memory ◽  
Memory Deficits ◽  
Hindlimb Unloading ◽  
Sprague Dawley ◽  
Negative Effects ◽  
Memory Impairments ◽  
Cholinergic Dysfunction ◽  
Sd Rats ◽  
And Oxidative Stress

The present study aimed to determine how the learning and memory gradually change with the prolonged hindlimb unloading (HU) treatment in rats. Different HU durations (7 d, 14 d, 21 d, and 28 d) in Sprague-Dawley (SD) rats were implemented. Cognitive function was assessed using the Morris water maze (MWM) and the shuttle box test. Additionally, parameters about cholinergic activity and oxidative stress were tested. Results showed that longer-than-14 d HU led to the inferior performances in the behavioral tasks. Besides, acetylcholine esterase (AChE) activity, malondialdehyde (MDA) level in brain, reactive oxygen species (ROS), and 8-hydroxy-2-deoxyguanosine (8-OHdG) concentrations of HU rats were significantly increased. Furthermore, choline acetyltransferase (ChAT), superoxide dismutase (SOD), and catalase (CAT) activity in brain were notably attenuated. Most of these effects were more pronounced after longer exposure (21 d and 28 d) to HU, although some indicators had their own characteristics of change. These results indicate that cholinergic dysfunction and oxidative damage were involved in the learning and memory impairments induced by longer-than-14 d HU. Moreover, the negative effects of HU tend to be augmented as the HU duration becomes longer. The results may be helpful to present possible biochemical targets for countermeasures development regarding the memory deficits under extreme environmental conditions.

scholarly journals Music Alleviates Learning and Memory Impairments in an Animal Model of Post-Traumatic Stress Disorder

2020 ◽  
Vol 11 (1) ◽  
pp. 7775-7784
Keyword(s):  
Learning And Memory ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Stressful Events ◽  
Post Traumatic Stress ◽  
Memory Impairments ◽  
Brain Functions ◽  
Male Wistar Rats ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) is the most prevalent disorder that occurs after experiencing life-threatening traumatic or stressful events. The most prevalent problems among PTSD patients are cognitive dysfunctions, including learning and memory impairments. Listening to music has constructive effects on brain functions, neurogenesis, and neuroplasticity, so the aim of the present study was to investigate the effect of music on learning and memory in a rat model of PTSD. Fifty-six adult male Wistar rats (200–250 gr) divided into four main groups (control, music, PTSD, and PTSD+ music) were used. A single prolonged stress (SPS) method was used for inducing PTSD in rats. Anxiety-like behaviors and Cognitive functions were evaluated using the Open field, Morris water maze (MWM), and passive avoidance test. Findings demonstrated that SPS induced marked impairment in learning and memory, and anxiolytic behaviors in rats and exposure to music significantly ameliorated these impairments. It seems that music can modulate the destructive effects of SPS on learning and memory at a behavioral level.

scholarly journals Neuroprotective Effects of Meloxicam and Selegiline in Scopolamine-Induced Cognitive Impairment and Oxidative Stress

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Puchchakayala Goverdhan ◽  
Akina Sravanthi ◽  
Thati Mamatha
Keyword(s):  
Learning And Memory ◽  
Neurodegenerative Disorder ◽  
Acetylcholinesterase Activity ◽  
Morris Water Maze Test ◽  
Therapeutic Effects ◽  
Neuroprotective Effects ◽  
Memory Impairments ◽  
Maze Test ◽  
Endogenous Antioxidant ◽  
Tbars Assay

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by a gradual decline in memory associated with shrinkage of brain tissue, with localized loss of neurons mainly in the hippocampus and basal forebrain, with diminished level of central cholinergic neurotransmitter-acetylcholine and also reported to be associated with accumulation of ubiquitinated proteins in neuronal inclusions and also with signs of inflammation. In these disorders, the abnormal protein aggregates may themselves trigger the expression of inflammatory mediators, such as cyclooxygenase 2 (COX-2). In the present study, the effects of Meloxicam, Selegiline, and coadministration of these drugs on scopolamine-induced learning and memory impairments in mice were investigated. Rectangular maze test, Morris water maze test, Locomotor activity, and Pole climbing test were conducted to evaluate the learning and memory parameters. Various biochemical parameters such as acetylcholinesterase(AChE), TBARS assay, catalase activity, and DPPH assay were also assessed. The present study demonstrates that Meloxicam, Selegiline, and co-administration of these test drugs had potential therapeutic effects on improving the antiamnesic activity in mice through inhibiting lipid peroxidation, augmenting endogenous antioxidant enzymes, and decreasing acetylcholinesterase activity in brain. The memory enhancing capacity of the drugs was very significant when compared to disease control (P<0.001).

scholarly journals A mini review of neuropharmacological effects of Rosa damascena Herrm.

2021 ◽  
Author(s):  
Farimah Beheshti ◽  
Somaieh Ahmadabady ◽  
Baghcheghi Yousef ◽  
Akbar Anaeigoudari ◽  
Mahmoud Hosseini
Keyword(s):  
Essential Oil ◽  
Learning And Memory ◽  
Sleep Disturbances ◽  
Epileptic Seizures ◽  
Rosa Damascena ◽  
Therapeutic Effects ◽  
Neuroprotective Effects ◽  
Memory Impairments ◽  
Scientific Databases ◽  
Rosaceae Family

Background: Rosa damascena Herrm (R. damascena) is a species of the Rosaceae family. The R. damascena has been shown to improve depression, anxiety and grief, it also suppresses allergic reactions and migraine headache. In addition, amelioration of learning and memory deficits, delay in onset of seizure attacks, alleviation of pain and improvement of sleep disorders have been attributed to extract and essential oil of R. damascena. This review was conducted to integrate the neuropharmacological effects of R. damascena. Methods: Employed scientific databases for collecting information were including PubMed, Web of Science, Scopus and Google Scholar. Results: The results of animal and clinical trial studies indicate that the extract of R. damascena and its essential oil apply useful therapeutic effects on depressant and anxiety- like behaviors, epileptic seizures, learning and memory impairments, sleep disturbances and pain. Conclusion: Based on scientific findings, the neuroprotective effects of R. damascena can be mainly linked to its antioxidant and anti-inflammatory properties.

scholarly journals Basolateral amygdala bidirectionally modulates stress-induced hippocampal learning and memory deficits through a p25/Cdk5-dependent pathway

2015 ◽  
Vol 112 (23) ◽  
pp. 7291-7296 ◽  
Author(s):  
Damien Rei ◽  
Xenos Mason ◽  
Jinsoo Seo ◽  
Johannes Gräff ◽  
Andrii Rudenko ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Glucocorticoid Receptors ◽  
Basolateral Amygdala ◽  
Neural Circuit ◽  
Dorsal Hippocampus ◽  
Memory Deficits ◽  
Memory Impairments ◽  
Repeated Stress ◽  
Learning And Memory Deficits ◽  
Necessary And Sufficient

Repeated stress has been suggested to underlie learning and memory deficits via the basolateral amygdala (BLA) and the hippocampus; however, the functional contribution of BLA inputs to the hippocampus and their molecular repercussions are not well understood. Here we show that repeated stress is accompanied by generation of the Cdk5 (cyclin-dependent kinase 5)-activator p25, up-regulation and phosphorylation of glucocorticoid receptors, increased HDAC2 expression, and reduced expression of memory-related genes in the hippocampus. A combination of optogenetic and pharmacosynthetic approaches shows that BLA activation is both necessary and sufficient for stress-associated molecular changes and memory impairments. Furthermore, we show that this effect relies on direct glutamatergic projections from the BLA to the dorsal hippocampus. Finally, we show that p25 generation is necessary for the stress-induced memory dysfunction. Taken together, our data provide a neural circuit model for stress-induced hippocampal memory deficits through BLA activity-dependent p25 generation.

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