Chronic cerebral hypoperfusion-induced memory impairment and hippocampal long-term potentiation deficits are improved by cholinergic stimulation in rats

2019 ◽  
Vol 71 (3) ◽  
pp. 443-448 ◽  
Author(s):  
Thenmoly Damodaran ◽  
Christian P. Müller ◽  
Zurina Hassan
Keyword(s):  
Memory Impairment ◽  
Long Term Potentiation ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Cholinergic Stimulation ◽  
Term Potentiation

scholarly journals Embelin Improves the Spatial Memory and Hippocampal Long-Term Potentiation in a Rat Model of Chronic Cerebral Hypoperfusion

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Saatheeyavaane Bhuvanendran ◽  
Siti Najmi Syuhadaa Bakar ◽  
Yatinesh Kumari ◽  
Iekhsan Othman ◽  
Mohd. Farooq Shaikh ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Spatial Memory ◽  
Rat Model ◽  
Long Term Potentiation ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Mrna Levels ◽  
Post Surgery ◽  
Term Potentiation

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.

Long-term potentiation saturation in chronic cerebral hypoperfusion

1998 ◽  
Vol 5 (3) ◽  
pp. 323-328 ◽  
Author(s):  
Lali H.S Sekhon ◽  
Ian Spence ◽  
Michael K Morgan ◽  
Neville C Weber
Keyword(s):  
Long Term Potentiation ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Term Potentiation

Chronic Cerebral Hypoperfusion Inhibits Calcium-Induced Long-term Potentiation in Rats

Stroke ◽  
1997 ◽  
Vol 28 (5) ◽  
pp. 1043-1048 ◽  
Author(s):  
Lali H. S. Sekhon ◽  
Ian Spence ◽  
Michael K. Morgan ◽  
Neville C. Weber
Keyword(s):  
Long Term Potentiation ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Term Potentiation

scholarly journals LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Daniela Puzzo ◽  
Roberto Piacentini ◽  
Mauro Fá ◽  
Walter Gulisano ◽  
Domenica D Li Puma ◽  
...  
Keyword(s):  
Associative Memory ◽  
Memory Impairment ◽  
Long Term Potentiation ◽  
Neuronal Uptake ◽  
Common Mechanism ◽  
Tau Oligomers ◽  
Term Potentiation ◽  
Induced Defects ◽  
Oligomeric Forms

The concurrent application of subtoxic doses of soluble oligomeric forms of human amyloid-beta (oAβ) and Tau (oTau) proteins impairs memory and its electrophysiological surrogate long-term potentiation (LTP), effects that may be mediated by intra-neuronal oligomers uptake. Intrigued by these findings, we investigated whether oAβ and oTau share a common mechanism when they impair memory and LTP in mice. We found that as already shown for oAβ, also oTau can bind to amyloid precursor protein (APP). Moreover, efficient intra-neuronal uptake of oAβ and oTau requires expression of APP. Finally, the toxic effect of both extracellular oAβ and oTau on memory and LTP is dependent upon APP since APP-KO mice were resistant to oAβ- and oTau-induced defects in spatial/associative memory and LTP. Thus, APP might serve as a common therapeutic target against Alzheimer's Disease (AD) and a host of other neurodegenerative diseases characterized by abnormal levels of Aβ and/or Tau.

Dopaminergic neurotransmission dysfunction induced by amyloid-β transforms cortical long-term potentiation into long-term depression and produces memory impairment

2016 ◽  
Vol 41 ◽  
pp. 187-199 ◽  
Author(s):  
Perla Moreno-Castilla ◽  
Luis F. Rodriguez-Duran ◽  
Kioko Guzman-Ramos ◽  
Alejandro Barcenas-Femat ◽  
Martha L. Escobar ◽  
...  
Keyword(s):  
Memory Impairment ◽  
Amyloid Β ◽  
Long Term Potentiation ◽  
Long Term Depression ◽  
Dopaminergic Neurotransmission ◽  
Term Potentiation

scholarly journals Spermidine protects from age-related synaptic alterations at hippocampal mossy fiber-CA3 synapses

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Marta Maglione ◽  
Gaga Kochlamazashvili ◽  
Tobias Eisenberg ◽  
Bence Rácz ◽  
Eva Michael ◽  
...  
Keyword(s):  
Molecular Basis ◽  
Memory Impairment ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Age Related ◽  
Term Potentiation ◽  
Hippocampal Synapses ◽  
Age Dependent ◽  
Age Related Changes

AbstractAging is associated with functional alterations of synapses thought to contribute to age-dependent memory impairment (AMI). While therapeutic avenues to protect from AMI are largely elusive, supplementation of spermidine, a polyamine normally declining with age, has been shown to restore defective proteostasis and to protect from AMI in Drosophila. Here we demonstrate that dietary spermidine protects from age-related synaptic alterations at hippocampal mossy fiber (MF)-CA3 synapses and prevents the aging-induced loss of neuronal mitochondria. Dietary spermidine rescued age-dependent decreases in synaptic vesicle density and largely restored defective presynaptic MF-CA3 long-term potentiation (LTP) at MF-CA3 synapses (MF-CA3) in aged animals. In contrast, spermidine failed to protect CA3-CA1 hippocampal synapses characterized by postsynaptic LTP from age-related changes in function and morphology. Our data demonstrate that dietary spermidine attenuates age-associated deterioration of MF-CA3 synaptic transmission and plasticity. These findings provide a physiological and molecular basis for the future therapeutic usage of spermidine.

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