Activation of endocannabinoid system in the rat basolateral amygdala improved scopolamine-induced memory consolidation impairment

Nedaei, Seyed Ershad; Rezayof, Ameneh; Pourmotabbed, Ali; Nasehi, Mohammad; Zarrindast, Mohammad‐Reza

doi:10.1016/j.bbr.2016.05.043

Cited by 15 publications

(8 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Scopolamine-induced amnesia is also characterized by an increased activity of AChE, which interferes with learning and memory by hydrolysing the neurotransmitter ACh into choline and acetic acid (Gautam et al, 2016;Kulshreshtha and Piplani, 2016;Nedaei et al, 2016). In the present study, KJH-1002 did not inhibit the increased AChE activity caused by scopolamine, indicating that cognitive function enhancement by KJH-1002 is not dependent on inhibition of AChE activity.…”

Section: Discussioncontrasting

confidence: 51%

“…All treatments were given by gavage, once daily in a volume of 10 mL•kg À1 . The group size for each experiment was determined by referring to previous studies (Moosavi et al, 2012;Li et al, 2016;Nedaei et al, 2016) using similar protocols to those of the present study. At least five independent samples are needed to detect significant differences between groups.…”

Section: Grouping and Pretreatmentmentioning

confidence: 99%

“…Alzheimer's disease (AD), defined as the progressive and irreversible decline of cognitive function, is the most prevalent form of dementia. Deficits in memory and learning are typical features of AD patients, and cognitive impairment is attributed to a marked loss of cholinergic neurons and decreased levels of ACh, via AChE (Nedaei et al, 2016). Oxidative stress is another crucial neurodegenerative disorder factor in AD patients (Gella and Durany, 2009;Bonda et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The phosphodiesterase 5 inhibitor, KJH‐1002, reverses a mouse model of amnesia by activating a cGMP/cAMP response element binding protein pathway and decreasing oxidative damage

Zhang

Seo

et al. 2018

British J Pharmacology

View full text Add to dashboard Cite

show abstract

Section: Discussioncontrasting

confidence: 51%

Section: Grouping and Pretreatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The phosphodiesterase 5 inhibitor, KJH‐1002, reverses a mouse model of amnesia by activating a cGMP/cAMP response element binding protein pathway and decreasing oxidative damage

Zhang

Seo

et al. 2018

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Some authors suggested that acetylcholine influences acquisition of new information differently from post-acquisition processes (Hasselmo and McGaughy, 2004;Meeter et al, 2004). Post-training administration of scopolamine was shown to impair performance in various spatial and non-spatial tasks (Doguc et al, 2012;Nedaei et al, 2016;Shi et al, 2013). Notably in respect to the present study, there are some indications that post-acquisition effects of cholinergic drugs might depend on the form of memory and learning investigated.…”

Section: Introductionsupporting

confidence: 38%

Differential effects of post-training scopolamine on spatial and non-spatial learning tasks in mice

Thonnard

Callaerts-Végh

D’Hooge

2019

Brain Research Bulletin

View full text Add to dashboard Cite

Muscarinic antagonist scopolamine has been extensively used to model amnesia in lab rodents, but most studies have focused on the effects of pre-training scopolamine administration. Here, we examined post-training scopolamine administration in C57BL/6JRj mice. Learning was assessed in three different procedures: odor discrimination in a digging paradigm, visual discrimination in a touchscreen-based setup, and spatial learning in the Morris water maze. Scopolamine administration affected performance in the odor discrimination task. More specifically, scopolamine decreased perseverance, which facilitated reversal learning. Similar results were obtained in the visual discrimination task, but scopolamine did not affect performance in the spatial learning task. It is unlikely that these results can be explained by non-memory-related cognitive effects (e.g., attention), non-cognitive behaviours (e.g., locomotor activity) or peripheral side-effects (e.g., mydriasis). They likely relate to the various neuropharmacological actions of scopolamine.

show abstract

“…Conversely, the microinjection of arachidonylcyclopropylamide (1-4 ng/rat), a CB1R agonist, into the rat's basolateral amygdala ameliorated a scopolamine-induced memory consolidation deficit (Nedaei et al, 2016). Additionally, endocannabinoid signaling engaged dorsal striatum glucocorticoids by promoting memory consolidation in Wistar rats, as evidenced by enhanced retention avoidance following inhibitory avoidance training (Siller-Pérez et al, 2019).…”

Section: Endocannabinoid System and Cognitive Abilitiesmentioning

confidence: 99%

Regulatory role of the endocannabinoid system on glial cells toward cognitive function in Alzheimer’s disease: A systematic review and meta-analysis of animal studies

et al. 2023

View full text Add to dashboard Cite

Objective: Over the last decade, researchers have sought to develop novel medications against dementia. One potential agent under investigation is cannabinoids. This review systematically appraised and meta-analyzed published pre-clinical research on the mechanism of endocannabinoid system modulation in glial cells and their effects on cognitive function in animal models of Alzheimer’s disease (AD).Methods: A systematic review complying with PRISMA guidelines was conducted. Six databases were searched: EBSCOHost, Scopus, PubMed, CINAHL, Cochrane, and Web of Science, using the keywords AD, cannabinoid, glial cells, and cognition. The methodological quality of each selected pre-clinical study was evaluated using the SYRCLE risk of bias tool. A random-effects model was applied to analyze the data and calculate the effect size, while I2 and p-values were used to assess heterogeneity.Results: The analysis included 26 original articles describing (1050 rodents) with AD-like symptoms. Rodents treated with cannabinoid agonists showed significant reductions in escape latency (standard mean difference [SMD] = −1.26; 95% confidence interval [CI]: −1.77 to −0.76, p < 0.00001) and ability to discriminate novel objects (SMD = 1.40; 95% CI: 1.04 to 1.76, p < 0.00001) compared to the control group. Furthermore, a significant decrease in Aβ plaques (SMD = −0.91; 95% CI: −1.55 to −0.27, p = 0.006) was observed in the endocannabinoid-treated group compared to the control group. Trends were observed toward neuroprotection, as represented by decreased levels of glial cell markers including glial fibrillary acid protein (SMD = −1.47; 95% CI: −2.56 to −0.38, p = 0.008) and Iba1 (SMD = −1.67; 95% CI: −2.56 to −0.79, p = 0.0002). Studies on the wild-type mice demonstrated significantly decreased levels of pro-inflammatory markers TNF-α, IL-1, and IL-6 (SMD = −2.28; 95% CI: −3.15 to −1.41, p = 0.00001). Despite the non-significant decrease in pro-inflammatory marker levels in transgenic mice (SMD = −0.47; 95% CI: −1.03 to 0.08, p = 0.09), the result favored the endocannabinoid-treated group over the control group.Conclusion: The revised data suggested that endocannabinoid stimulation promotes cognitive function via modulation of glial cells by decreasing pro-inflammatory markers in AD-like rodent models. Thus, cannabinoid agents may be required to modulate the downstream chain of effect to enhance cognitive stability against concurrent neuroinflammation in AD. Population-based studies and well-designed clinical trials are required to characterize the acceptability and real-world effectiveness of cannabinoid agents.Systematic Review Registration: [https://inplasy.com/inplasy-2022-8-0094/], identifier [Inplasy Protocol 3770].

show abstract

Activation of endocannabinoid system in the rat basolateral amygdala improved scopolamine-induced memory consolidation impairment

Cited by 15 publications

References 72 publications

The phosphodiesterase 5 inhibitor, KJH‐1002, reverses a mouse model of amnesia by activating a cGMP/cAMP response element binding protein pathway and decreasing oxidative damage

The phosphodiesterase 5 inhibitor, KJH‐1002, reverses a mouse model of amnesia by activating a cGMP/cAMP response element binding protein pathway and decreasing oxidative damage

Differential effects of post-training scopolamine on spatial and non-spatial learning tasks in mice

Regulatory role of the endocannabinoid system on glial cells toward cognitive function in Alzheimer’s disease: A systematic review and meta-analysis of animal studies

Contact Info

Product

Resources

About