scholarly journals Doxorubicin induces dysregulation of AMPA receptor and impairs hippocampal synaptic plasticity leading to learning and memory deficits

Heliyon ◽  
2021 ◽  
pp. e07456
Author(s):  
Ahmad H. Alhowail ◽  
Priyanka D. Pinky ◽  
Matthew Eggert ◽  
Jenna Bloemer ◽  
Lauren N. Woodie ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Ampa Receptor ◽  
Memory Deficits ◽  
Hippocampal Synaptic Plasticity ◽  
Learning And Memory Deficits

scholarly journals Electroacupuncture Ameliorates Learning and Memory and Improves Synaptic Plasticity via Activation of the PKA/CREB Signaling Pathway in Cerebral Hypoperfusion

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Cai-Xia Zheng ◽  
Min Lu ◽  
Ya-Bi Guo ◽  
Feng-Xia Zhang ◽  
Hua Liu ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Signaling Pathway ◽  
Learning And Memory ◽  
Molecular Mechanisms ◽  
Memory Deficits ◽  
Long Term Potentiation ◽  
Cerebral Hypoperfusion ◽  
Electrophysiological Recording ◽  
Learning And Memory Deficits ◽  
Creb Pathway

Electroacupuncture (EA) has shown protective effects on cognitive decline. However, the underlying molecular mechanisms are ill-understood. The present study was undertaken to determine whether the cognitive function was ameliorated in cerebral hypoperfusion rats following EA and to investigate the role of PKA/CREB pathway. We used a rat 2-vessel occlusion (2VO) model and delivered EA at Baihui (GV20) and Dazhui (GV14) acupoints. Morris water maze (MWM) task, electrophysiological recording, Golgi silver stain, Nissl stain, Western blot, and real-time PCR were employed. EA significantly (1) ameliorated the spatial learning and memory deficits, (2) alleviated long-term potentiation (LTP) impairment and the reduction of dendritic spine density, (3) suppressed the decline of phospho-CREB (pCREB) protein, brain-derived neurotrophic factor (BDNF) protein, and microRNA132 (miR132), and (4) reduced the increase of p250GAP protein of 2VO rats. These changes were partially blocked by a selective protein kinase A (PKA) inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H89), suggesting that the PKA/CREB pathway is potentially involved in the effects of EA. Moreover, any significant damage to the pyramidal cell layer of CA1 subregion was absent. These results demonstrated that EA could ameliorate learning and memory deficits and alleviate hippocampal synaptic plasticity impairment of cerebral hypoperfusion rats, potentially mediated by PKA/CREB signaling pathway.

Dihydroartemisinin Induces O-GlcNAcylation and Improves Cognitive Function in a Mouse Model of Tauopathy

2021 ◽  
pp. 1-10
Author(s):  
Lei Xia ◽  
Yayan Pang ◽  
Junjie Li ◽  
Bin Wu ◽  
Yehong Du ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Mouse Model ◽  
Learning And Memory ◽  
Protein Misfolding ◽  
Memory Deficits ◽  
Long Term Potentiation ◽  
Electrophysiological Recording ◽  
Tau Pathology ◽  
Neuroprotective Effects ◽  
Learning And Memory Deficits

Background: Tauopathies are a group of neurodegenerative disorders, including Alzheimer’s disease (AD) and frontotemporal lobar degeneration with tau pathology. Hyperphosphorylation modification promotes tau protein misfolding and aggregation into neurofibrillary tangles, leading to impairments of synaptic plasticity and learning and memory. However, very limited therapeutic strategies are available. Objective: In the present study, we wanted to investigate the potential effects of Dihydroartemisinin (DHA) on tauopathies. Methods: We constructed adeno-associated virus carrying hTau cDNA (AAVhTau) to establish a mouse model of tauopathy through intrahippocampal microinjection. Using a combination of behavioral test, electrophysiological recording, and western blotting assay, we examined the neuroprotective effects of DHA on learning and memory deficits in mice with tauopathy. Results: DHA improved learning and memory and increased hippocampal CA1 long-term potentiation (LTP) in mice overexpressed human tau (hTau) in the hippocampus. More importantly, further study revealed that DHA could induce protein O-GlcNAcylation modification and reduce protein phosphorylation. O-GlcNAc transferase inhibitor alloxan could suppress DHA-induced protein O-GlcNAcylation, and subsequently prevent therapeutic effect of DHA on the deficits of learning and memory as well as synaptic plasticity in hTau mice. Conclusion: These results indicate that DHA may exert neuroprotective role in tauopathy through a crosstalk between O-GlcNAcylation and phosphorylation, suggesting a potential therapeutic for learning and memory deficits associated with tau pathology.

Levodopa ameliorates learning and memory deficits in a murine model of Alzheimer’s disease

2009 ◽  
Vol 30 (8) ◽  
pp. 1192-1204 ◽  
Author(s):  
Oliver Ambrée ◽  
Helene Richter ◽  
Norbert Sachser ◽  
Lars Lewejohann ◽  
Ekrem Dere ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Learning And Memory ◽  
Murine Model ◽  
Memory Deficits ◽  
Model Of Alzheimer’S Disease ◽  
Learning And Memory Deficits
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