Rapamycin, by Inhibiting mTORC1 Signaling, Prevents the Loss of Striatal Bidirectional Synaptic Plasticity in a Rat Model of L-DOPA-Induced Dyskinesia

Abstract Alzheimer’s disease (AD) is the second most occurring neurological disorder after stroke and is associated with cerebral hypoperfusion, possibly contributing to cognitive impairment. In the present study, neuroprotective and anti-AD effects of embelin were evaluated in chronic cerebral hypoperfusion (CCH) rat model using permanent bilateral common carotid artery occlusion (BCCAO) method. Rats were administered with embelin at doses of 0.3, 0.6 or 1.2 mg/kg (i.p) on day 14 post-surgery and tested in Morris water maze (MWM) followed by electrophysiological recordings to access cognitive abilities and synaptic plasticity. The hippocampal brain regions were extracted for gene expression and neurotransmitters analysis. Treatment with embelin at the doses of 0.3 and 0.6 mg/kg significantly reversed the spatial memory impairment induced by CCH in rats. Embelin treatment has significantly protected synaptic plasticity impairment as assessed by hippocampal long-term potentiation (LTP) test. The mechanism of this study demonstrated that embelin treatment alleviated the decreased expression of BDNF, CREB1, APP, Mapt, SOD1 and NFκB mRNA levels caused by CCH rats. Furthermore, treatment with embelin demonstrated neuromodulatory activity by its ability to restore hippocampal neurotransmitters. Overall these data suggest that embelin improve memory and synaptic plasticity impairment in CCH rats and can be a potential drug candidate for neurodegenerative disease-related cognitive disorders.

Download Full-text

Neurotoxic effects of high-dose piperine on hippocampal synaptic transmission and synaptic plasticity in a rat model of memory impairment

NeuroToxicology ◽

10.1016/j.neuro.2020.04.008 ◽

2020 ◽

Vol 79 ◽

pp. 200-208 ◽

Cited By ~ 1

Author(s):

Masoomeh Nazifi ◽

Manoochehr Ashrafpoor ◽

Shahrbanoo Oryan ◽

Delaram Eslimi Esfahani ◽

Ali Akbar Moghadamnia

Keyword(s):

Synaptic Plasticity ◽

Synaptic Transmission ◽

Rat Model ◽

Memory Impairment ◽

High Dose ◽

Neurotoxic Effects

Download Full-text

NR2B-Tyr phosphorylation regulates synaptic plasticity in central sensitization in a chronic migraine rat model

The Journal of Headache and Pain ◽

10.1186/s10194-018-0935-2 ◽

2018 ◽

Vol 19 (1) ◽

Cited By ~ 18

Author(s):

Xue-Ying Wang ◽

Hui-Ru Zhou ◽

Sha Wang ◽

Chao-Yang Liu ◽

Guang-Cheng Qin ◽

...

Keyword(s):

Synaptic Plasticity ◽

Chronic Migraine ◽

Rat Model ◽

Central Sensitization

Download Full-text

Impaired ILK Function Is Associated with Deficits in Hippocampal Based Memory and Synaptic Plasticity in a FASD Rat Model

PLoS ONE ◽

10.1371/journal.pone.0135700 ◽

2015 ◽

Vol 10 (8) ◽

pp. e0135700 ◽

Cited By ~ 12

Author(s):

D. Bhattacharya ◽

E. P. Dunaway ◽

S. Bhattacharya ◽

J. Bloemer ◽

M. Buabeid ◽

...

Keyword(s):

Synaptic Plasticity ◽

Rat Model

Download Full-text

Correction to: Moderate Treadmill Exercise Protects Synaptic Plasticity of the Dentate Gyrus and Related Signaling Cascade in a Rat Model of Alzheimer’s Disease

Molecular Neurobiology ◽

10.1007/s12035-017-0788-8 ◽

2017 ◽

Vol 55 (1) ◽

pp. 901-901

Author(s):

An T. Dao ◽

Munder A. Zagaar ◽

Karim A. Alkadhi

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Synaptic Plasticity ◽

Dentate Gyrus ◽

Rat Model ◽

Treadmill Exercise ◽

Signaling Cascade ◽

Model Of Alzheimer’S Disease

Download Full-text

Environmental Enrichment Protects Offspring of a Rat Model of Preeclampsia from Cognitive Decline

10.21203/rs.3.rs-736215/v1 ◽

2021 ◽

Author(s):

Huiqing Lu ◽

Lili Gong ◽

Huangfang Xu ◽

Qiongjie Zhou ◽

Huanqiang Zhao ◽

...

Keyword(s):

Synaptic Plasticity ◽

Cognitive Ability ◽

Inflammatory Cytokines ◽

Spatial Learning ◽

Rat Model ◽

Environmental Enrichment ◽

Inflammatory Cytokine ◽

Hippocampal Neurogenesis ◽

Expression Levels ◽

Cytokine Levels

Abstract Background Preeclampsia affects 5–8% of all pregnancies and contributes to adverse pregnancy and birth outcomes. In addition to the short-term effects of preeclampsia, preeclampsia can exert long-term adverse effects on offspring. Numerous studies have demonstrated that offspring of preeclamptic women exhibit cognitive deficits from childhood to old age. However, effective ways to improve the cognitive abilities of these offspring remain to be investigated. The aim of this study was to explore whether environmental enrichment in early life could restore the cognitive ability of the offspring of a rat model of preeclampsia and to investigate the cellular and molecular mechanisms by which EE improves cognitive ability. Methods L-NAME was used to establish a rat model of preeclampsia. The spatial learning and memory abilities and recognition memory of 56-day-old offspring were evaluated by the Morris water maze and Novel object recognition (NOR) task. Immunofluorescence was performed to evaluate cell proliferation and apoptosis in the DG region of the hippocampus. qRT-PCR was performed to examine the expression levels of neurogenesis-associated genes, pre- and postsynaptic proteins and inflammatory cytokines. An enzyme-linked immune absorbent assay was performed to evaluate the concentration of vascular endothelial growth factor (VEGF) and inflammatory cytokines in the hippocampus. Results The administration of L-NAME led to increased systolic blood pressure and urine protein levels in pregnant rats. Offspring in the L-NAME group exhibited impaired spatial learning ability and memory as well as NOR memory. Hippocampal neurogenesis and synaptic plasticity were impaired in offspring from the L-NAME group. Furthermore, cell apoptosis in the hippocampus was increased in the L-NAME group. The hippocampus was skewed to a proinflammatory profile, as shown by increased inflammatory cytokine levels. EE improved the cognitive ability of offspring in the L-NAME group and resulted in increased hippocampal neurogenesis and synaptic protein expression levels and decreased apoptosis and inflammatory cytokine levels. Conclusions Environmental enrichment resolves cognitive impairment in the offspring of a rat model of preeclampsia by improving hippocampal neurogenesis and synaptic plasticity and normalizing the apoptosis level and the inflammatory balance.

Download Full-text