Exendin-4 Improves Long-Term Potentiation and Neuronal Dendritic Growth in High-Fat Diet Mice and Neurons Under Metabolic Imbalance Conditions

2020 ◽  
Author(s):  
Juhyun Song ◽  
Ming Wang ◽  
Gwangho Yoon ◽  
Jihoon Jo
Keyword(s):  
Metabolic Syndrome ◽  
Synaptic Plasticity ◽  
High Fat Diet ◽  
Long Term Potentiation ◽  
Lifestyle Changes ◽  
High Fat ◽  
Metabolism Regulation ◽  
Term Potentiation ◽  
Metabolic Imbalance

Abstract Metabolic syndrome, which increases the risk of obesity and type 2 diabetes, has emerged as a significant issue worldwide. Metabolic syndrome can occur due to diverse factors such as genetic background, lifestyle changes, food intake, and aging. Recent studies have highlighted the relationship between metabolic imbalance and neurological pathologies, such as synaptic dysfunction and memory loss. Glucagon-like peptide 1 (GLP-1) secreted from gut L-cells, and specific brain nuclei play multiple roles, including glucose metabolism, regulation of insulin sensitivity, inflammation control, synaptic plasticity improvement, and neuronal protection. Even though GLP-1 and GLP-1 receptor agonists (GLP-1RA) appear to have neuroprotective functions, the specific mechanisms of GLP-1 and GLP-1RA in brain function have remained unclear. Here, we investigated whether exendin-4 improves cognitive function and brain insulin resistance in metabolic imbalanced high-fat diet mice brain as a GLP-1RA, using electrophysiological experiments. Further, we identified the neuroprotective effect of exendin-4 in primary cultured hippocampal and cortical neurons under an in vitro metabolic imbalance condition, including neuronal structure improvement. This study provides significant findings on the effects of exendin-4 in synaptic plasticity, long-term potentiation (LTP), neuroinflammation, and neural structure. We suggest that GLP-1 may be vital to treating neuropathology caused by metabolic imbalance.

scholarly journals Exendin-4 improves long-term potentiation and neuronal dendritic growth in vivo and in vitro obesity condition

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ming Wang ◽  
Gwangho Yoon ◽  
Juhyun Song ◽  
Jihoon Jo
Keyword(s):  
Metabolic Syndrome ◽  
Synaptic Plasticity ◽  
Cortical Neurons ◽  
High Fat Diet ◽  
Neuroprotective Effect ◽  
Long Term Potentiation ◽  
High Fat ◽  
Term Potentiation

AbstractMetabolic syndrome, which increases the risk of obesity and type 2 diabetes has emerged as a significant issue worldwide. Recent studies have highlighted the relationship between metabolic imbalance and neurological pathologies such as memory loss. Glucagon-like peptide 1 (GLP-1) secreted from gut L-cells and specific brain nuclei plays multiple roles including regulation of insulin sensitivity, inflammation and synaptic plasticity. Although GLP-1 and GLP-1 receptor agonists appear to have neuroprotective function, the specific mechanism of their action in brain remains unclear. We investigated whether exendin-4, as a GLP-1RA, improves cognitive function and brain insulin resistance in metabolic-imbalanced mice fed a high-fat diet. Considering the result of electrophysiological experiments, exendin-4 inhibits the reduction of long term potentiation (LTP) in high fat diet mouse brain. Further, we identified the neuroprotective effect of exendin-4 in primary cultured hippocampal and cortical neurons in in vitro metabolic imbalanced condition. Our results showed the improvement of IRS-1 phosphorylation, neuronal complexity, and the mature of dendritic spine shape by exendin-4 treatment in metabolic imbalanced in vitro condition. Here, we provides significant evidences on the effect of exendin-4 on synaptic plasticity, long-term potentiation, and neural structure. We suggest that GLP-1 is important to treat neuropathology caused by metabolic syndrome.

scholarly journals High fat diet treatment impairs hippocampal long-term potentiation without alterations of the core neuropathological features of Alzheimer disease

2018 ◽  
Vol 113 ◽  
pp. 82-96 ◽  
Author(s):  
Isabel H. Salas ◽  
Akila Weerasekera ◽  
Tariq Ahmed ◽  
Zsuzsanna Callaerts-Vegh ◽  
Uwe Himmelreich ◽  
...  
Keyword(s):  
Alzheimer Disease ◽  
High Fat Diet ◽  
Long Term Potentiation ◽  
High Fat ◽  
The Core ◽  
Diet Treatment ◽  
Term Potentiation

Effect of high-fat diet and antioxidants on hippocampal long-term potentiation in rats: An in vivo study

2013 ◽  
Vol 1539 ◽  
pp. 1-6 ◽  
Author(s):  
Seyed Asaad Karimi ◽  
Iraj Salehi ◽  
Alireza Komaki ◽  
Abdolrahman Sarihi ◽  
Mohammad Zarei ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Long Term Potentiation ◽  
In Vivo Study ◽  
High Fat ◽  
Term Potentiation

scholarly journals Effects of the hydroalcoholic extract of Rosa damascena on hippocampal long-term potentiation in rats fed high-fat diet

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Seyed Asaad Karimi ◽  
Somayeh Komaki ◽  
Masoumeh Taheri ◽  
Ghazaleh Omidi ◽  
Masoumeh Kourosh-Arami ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Rosa Damascena ◽  
High Fat ◽  
Oxidative Stress Biomarkers ◽  
Hydroalcoholic Extract ◽  
Hippocampal Synaptic Plasticity ◽  
Term Potentiation

AbstractHigh-fat diets (HFDs) and obesity can cause serious health problems, such as neurodegenerative diseases and cognitive impairments. Consumption of HFD is associated with reduction in hippocampal synaptic plasticity. Rosa damascena (R. damascena) is traditionally used as a dietary supplement for many disorders. This study was carried out to determine the beneficial effect of hydroalcoholic extract of R. damascena on in vivo hippocampal synaptic plasticity (long-term potentiation, LTP) in the perforant pathway (PP)—dentate gyrus (DG) pathway in rats fed with an HFD. Male Wistar rats were randomly assigned to four groups: Control, R. damascena extract (1 g/kg bw daily for 30 days), HFD (for 90 days) and HFD + extract. The population spike (PS) amplitude and slope of excitatory post-synaptic potentials (EPSP) were measured in DG area in response to stimulation applied to the PP. Serum oxidative stress biomarkers [total thiol group (TTG) and superoxide dismutase (SOD)] were measured. The results showed the HFD impaired LTP induction in the PP-DG synapses. This conclusion is supported by decreased EPSP slope and PS amplitude of LTP. R. damascena supplementation in HFD animals enhanced EPSP slope and PS amplitude of LTP in the granular cell of DG. Consumption of HFD decreased TTG and SOD. R. damascena extract consumption in the HFD animals enhanced TTG and SOD. These data indicate that R. damascena dietary supplementation can ameliorate HFD-induced alteration of synaptic plasticity, probably through its significant antioxidant effects and activate signalling pathways, which are critical in controlling synaptic plasticity.

Neuroprotective effects of metformin against Aβ-mediated inhibition of long-term potentiation in rats fed a high-fat diet

2016 ◽  
Vol 121 ◽  
pp. 178-185 ◽  
Author(s):  
Masoumeh Asadbegi ◽  
Parichehreh Yaghmaei ◽  
Iraj Salehi ◽  
Azadeh Ebrahim-Habibi ◽  
Alireza Komaki
Keyword(s):  
High Fat Diet ◽  
Long Term Potentiation ◽  
High Fat ◽  
Neuroprotective Effects ◽  
Term Potentiation

Effect of garlic powder on hippocampal long-term potentiation in rats fed high fat diet: an in vivo study

2018 ◽  
Vol 33 (3) ◽  
pp. 725-731 ◽  
Author(s):  
Iraj Salehi ◽  
Alireza Komaki ◽  
Seyed Asaad Karimi ◽  
Abdolrahman Sarihi ◽  
Mohammad Zarei
Keyword(s):  
High Fat Diet ◽  
Long Term Potentiation ◽  
In Vivo Study ◽  
High Fat ◽  
Garlic Powder ◽  
Term Potentiation

scholarly journals Study of thymol effect on Aß inhibition of long-term potentiation (LTP) in rats receiving a high fat diet

2016 ◽  
Vol 10 ◽  
Author(s):  
Asadbegi(hamedi) Masoumeh ◽  
Komaki Alireza ◽  
Yaghmaei Parichehr ◽  
Habibi Azadeh ◽  
Salehi Iraj
Keyword(s):  
High Fat Diet ◽  
Long Term Potentiation ◽  
High Fat ◽  
Term Potentiation

Brivaracetam Prevents the Over-expression of Synaptic Vesicle Protein 2A and Rescues the Deficits of Hippocampal Long-term Potentiation In Vivo in Chronic Temporal Lobe Epilepsy Rats

2020 ◽  
Vol 17 (4) ◽  
pp. 354-360 ◽  
Author(s):  
Yu-Xing Ge ◽  
Ying-Ying Lin ◽  
Qian-Qian Bi ◽  
Yu-Juan Chen
Keyword(s):  
Synaptic Plasticity ◽  
Temporal Lobe Epilepsy ◽  
Synaptic Vesicle ◽  
Long Term Potentiation ◽  
Synaptic Dysfunction ◽  
Over Expression ◽  
Term Potentiation ◽  
Synaptic Vesicle Protein 2A

Background: Patients with temporal lobe epilepsy (TLE) usually suffer from cognitive deficits and recurrent seizures. Brivaracetam (BRV) is a novel anti-epileptic drug (AEDs) recently used for the treatment of partial seizures with or without secondary generalization. Different from other AEDs, BRV has some favorable properties on synaptic plasticity. However, the underlying mechanisms remain elusive. Objective: The aim of this study was to explore the neuroprotective mechanism of BRV on synaptic plasticity in experimental TLE rats. Methods: The effect of chronic treatment with BRV (10 mg/kg) was assessed on Pilocarpine induced TLE model through measurement of the field excitatory postsynaptic potentials (fEPSPs) in vivo. Differentially expressed synaptic vesicle protein 2A (SV2A) were identified with immunoblot. Then, fast phosphorylation of synaptosomal-associated protein 25 (SNAP-25) during long-term potentiation (LTP) induction was performed to investigate the potential roles of BRV on synaptic plasticity in the TLE model. Results: An increased level of SV2A accompanied by a depressed LTP in the hippocampus was shown in epileptic rats. Furthermore, BRV treatment continued for more than 30 days improved the over-expression of SV2A and reversed the synaptic dysfunction in epileptic rats. Additionally, BRV treatment alleviates the abnormal SNAP-25 phosphorylation at Ser187 during LTP induction in epileptic ones, which is relevant to the modulation of synaptic vesicles exocytosis and voltagegated calcium channels. Conclusion: BRV treatment ameliorated the over-expression of SV2A in the hippocampus and rescued the synaptic dysfunction in epileptic rats. These results identify the neuroprotective effect of BRV on TLE model.

Sign in / Sign up

Export Citation Format

Share Document