GPER1 Modulates Synaptic Plasticity During the Development of Temporal Lobe Epilepsy in Rats

Zhang, Xian; Yang, Yang; Zhou, Jian; Niu, Junfeng; Wang, Peng; Qiang, Ya‐Wei; Liu, Kunmei; Wen, Yujun; Zhang, Lianxiang; Wang, Rui

doi:10.1007/s11064-021-03336-8

Cited by 6 publications

(5 citation statements)

References 40 publications

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“…This rapidly appeared within minutes, while the major veins (inferior caval and superior mesenteric veins) appeared to be congested and the azygos vein failed. Furthermore, lithium may induce direct damage to the liver, kidneys [ 70 , 71 , 72 , 73 , 74 ], heart [ 75 , 76 ], lungs [ 77 , 78 ], and brain [ 79 , 80 ].…”

Section: Discussionmentioning

confidence: 99%

“…For the noted BPC 157-lithium activity, the specific “bypassing key”, which is a common point in vascular occlusion studies [ 2 , 3 , 4 , 5 , 6 , 7 , 8 ], absolute alcohol intragastric instillation occlusion-like peripheral and central syndrome [ 9 ], and in the lithium-treated rats, may represent the noted special interaction with the NO system and NO agents in the various models and species [ 36 ]. BPC 157 induced the release of NO on its own [ 81 , 82 ], counteracted the induced hypertension and pro-thrombotic effects (L-NAME) [ 79 , 81 ], and induced hypotension and anti-thrombotic (L-arginine) effects [ 83 , 84 ]). The specific effects on blood pressure and maintenance of thrombocyte function [ 38 , 81 , 83 , 84 ] is in accordance with the vasomotor tone carried out through the BPC 157-specific activation of the Src-caveolin-1-endothelial nitric oxide synthase (eNOS) pathway [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

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Over-Dose Lithium Toxicity as an Occlusive-like Syndrome in Rats and Gastric Pentadecapeptide BPC 157

et al. 2021

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Due to endothelial impairment, high-dose lithium may produce an occlusive-like syndrome, comparable to permanent occlusion of major vessel-induced syndromes in rats; intracranial, portal, and caval hypertension, and aortal hypotension; multi-organ dysfunction syndrome; brain, heart, lung, liver, kidney, and gastrointestinal lesions; arterial and venous thrombosis; and tissue oxidative stress. Stable gastric pentadecapeptide BPC 157 may be a means of therapy via activating loops (bypassing vessel occlusion) and counteracting major occlusion syndromes. Recently, BPC 157 counteracted the lithium sulfate regimen in rats (500 mg/kg/day, ip, for 3 days, with assessment at 210 min after each administration of lithium) and its severe syndrome (muscular weakness and prostration, reduced muscle fibers, myocardial infarction, and edema of various brain areas). Subsequently, BPC 157 also counteracted the lithium-induced occlusive-like syndrome; rapidly counteracted brain swelling and intracranial (superior sagittal sinus) hypertension, portal hypertension, and aortal hypotension, which otherwise would persist; counteracted vessel failure; abrogated congestion of the inferior caval and superior mesenteric veins; reversed azygos vein failure; and mitigated thrombosis (superior mesenteric vein and artery), congestion of the stomach, and major hemorrhagic lesions. Both regimens of BPC 157 administration also counteracted the previously described muscular weakness and prostration (as shown in microscopic and ECG recordings), myocardial congestion and infarction, in addition to edema and lesions in various brain areas; marked dilatation and central venous congestion in the liver; large areas of congestion and hemorrhage in the lung; and degeneration of proximal and distal tubules with cytoplasmic vacuolization in the kidney, attenuating oxidative stress. Thus, BPC 157 therapy overwhelmed high-dose lithium intoxication in rats.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Over-Dose Lithium Toxicity as an Occlusive-like Syndrome in Rats and Gastric Pentadecapeptide BPC 157

et al. 2021

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“…Moreover, TMX, a SERM, prevented the ischemia-induced neuronal damage in the hippocampus of male rats [278,279]. Additionally, G-1 and G-15, a GPER1 agonist and antagonist, respectively, modulated synaptic plasticity during temporal lobe epilepsy in Sprague Dawley rats [173]. However, E2 modulated hippocampal neurogenesis and cell death in adult female rats, but not in male rats [280,281].…”

Section: Neuroprotectionmentioning

confidence: 95%

“…G-1 is a GPER1 receptor agonist that mediates rapid signaling [171] (Figure 6E). G-1 was proven to be effective in preclinical studies regarding multiple sclerosis, ischemia, stroke, epilepsy, and brain injury [172][173][174]. However, in murine bone marrow mesenchymal stem cells and endometrium cells, G-1 had proliferative properties [175,176].…”

Section: Activators Of Non-genomic Estrogen-like Signaling (Angels)mentioning

confidence: 99%

Estradiol and Estrogen-like Alternative Therapies in Use: The Importance of the Selective and Non-Classical Actions

et al. 2022

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Estrogen is one of the most important female sex hormones, and is indispensable for reproduction. However, its role is much wider. Among others, due to its neuroprotective effects, estrogen protects the brain against dementia and complications of traumatic injury. Previously, it was used mainly as a therapeutic option for influencing the menstrual cycle and treating menopausal symptoms. Unfortunately, hormone replacement therapy might be associated with detrimental side effects, such as increased risk of stroke and breast cancer, raising concerns about its safety. Thus, tissue-selective and non-classical estrogen analogues have become the focus of interest. Here, we review the current knowledge about estrogen effects in a broader sense, and the possibility of using selective estrogen-receptor modulators (SERMs), selective estrogen-receptor downregulators (SERDs), phytoestrogens, and activators of non-genomic estrogen-like signaling (ANGELS) molecules as treatment.

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“…The Nissl staining procedure was conducted following the established protocol of the study [34] . The brain slice were immersed in Nissl staining solution at 56℃ for 1h, rinsed with deionized water and placed in the differentiation solution at room temperature until the background of the brain slice was nearly transparent.…”

Section: Nissl Stainingmentioning

confidence: 99%

Q2Ketogenic diets alter the Gut Microbiome resulting in decreased susceptibility and cognitive impairment of Pilocarpine-Induced status epilepticus

Li,

Ma,

Wang

et al. 2024

Preprint

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The ketogenic diet (KD) is a high-fat, low-carbohydrate, and low-protein dietary approach that exerts antiepileptogenic effects by attenuating spontaneous recurrent seizures, ameliorating learning and memory impairments, and modulating the gut microbiota composition. However, the role of gut microbiome in antiepileptic effects of KD on temporal lobe epilepsy (TLE) induced by lithium-pilocarpine in adult rats are still unknown. Our study provides evidence demonstrating that the KD effectively mitigates seizure behavior and reduces acute-phase epileptic brain activity, KD treatment alleviates hippocampal neuronal damage and improves cognitive impairment induced by TLE. We also observed that the beneficial effects of the KD are compromised when gut microbiota is disrupted through antibiotic administration. Components of gut microbiota analysis using 16S rRNA gene sequencing in fecal samples collected from TLE rats fed either KD or normal diet. Chao, ACE index showed a decrease species variety in KD treatment rats compared to TLE rats with normal diet. KD increased the level of Actinobacteriota, Verrucomicrobiota and Proteobacteria and decreased the level of Bacteroidetes. Interestingly, the abundance of Actinobacteriota and Verrucomicrobiota indicate a positive correlation with the learning and memory ability, the abundance of Proteobacteria showed a positive correlation with the seizure susceptibility. In conclusion, our study unveils the significant antiepileptic and neuroprotective effect of the KD in pilocarpine-induced epileptic rats, primarily mediated through the modulation of gut microbiota. However, gut microbiota mediates the anti-seizure effects of the KD still needs to be better elucidated.

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GPER1 Modulates Synaptic Plasticity During the Development of Temporal Lobe Epilepsy in Rats

Cited by 6 publications

References 40 publications

Over-Dose Lithium Toxicity as an Occlusive-like Syndrome in Rats and Gastric Pentadecapeptide BPC 157

Over-Dose Lithium Toxicity as an Occlusive-like Syndrome in Rats and Gastric Pentadecapeptide BPC 157

Estradiol and Estrogen-like Alternative Therapies in Use: The Importance of the Selective and Non-Classical Actions

Q2Ketogenic diets alter the Gut Microbiome resulting in decreased susceptibility and cognitive impairment of Pilocarpine-Induced status epilepticus

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