Subclinical Doses of ATP-Sensitive Potassium Channel Modulators Prevent Alterations in Memory and Synaptic Plasticity Induced by Amyloid-β

2017 ◽  
Vol 57 (1) ◽  
pp. 205-226 ◽  
Author(s):  
Karla Salgado-Puga ◽  
Javier Rodríguez-Colorado ◽  
Roberto A. Prado-Alcalá ◽  
Fernando Peña-Ortega
Keyword(s):  
Synaptic Plasticity ◽  
Potassium Channel ◽  
Amyloid Β ◽  
Potassium Channel Modulators

scholarly journals Effect of Potassium Channel Modulators on Morphine Withdrawal in Mice

2010 ◽  
Vol 4 ◽  
pp. SART.S6211 ◽  
Author(s):  
Vikas Seth ◽  
Mushtaq Ahmad ◽  
Prerna Upadhyaya ◽  
Monika Sharma ◽  
Vijay Moghe
Keyword(s):  
Potassium Channel ◽  
Withdrawal Syndrome ◽  
Channel Blocker ◽  
Inhibitory Effect ◽  
Morphine Withdrawal ◽  
The Other ◽  
Opioid Antagonist ◽  
Potassium Channel Openers ◽  
Potassium Channel Modulators ◽  
Withdrawal Signs

The present study was conducted to investigate the effect of potassium channel openers and blockers on morphine withdrawal syndrome. Mice were rendered dependent on morphine by subcutaneous injection of morphine; four hours later, withdrawal was induced by using an opioid antagonist, naloxone. Mice were observed for 30 minutes for the withdrawal signs ie, the characteristic jumping, hyperactivity, urination and diarrhea. ATP-dependent potassium (K+ATP) channel modulators were injected intraperitoneally (i.p.) 30 minutes before the naloxone. It was found that a K+ATP channel opener, minoxidil (12.5–50 mg/kg i.p.), suppressed the morphine withdrawal significantly. On the other hand, the K+ATP channel blocker glibenclamide (12.5–50 mg/kg i.p.) caused a significant facilitation of the withdrawal. Glibenclamide was also found to abolish the minoxidil's inhibitory effect on morphine withdrawal. The study concludes that K+ATP channels play an important role in the genesis of morphine withdrawal and K+ATP channel openers could be useful in the management of opioid withdrawal. As morphine opens K+ATP channels in neurons, the channel openers possibly act by mimicking the effects of morphine on neuronal K+ currents.

Multi-scale modeling of altered synaptic plasticity related to Amyloid β effects

2017 ◽  
Vol 93 ◽  
pp. 230-239 ◽  
Author(s):  
Takumi Matsuzawa ◽  
László Zalányi ◽  
Tamás Kiss ◽  
Péter Érdi
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β ◽  
Multi Scale ◽  
Scale Modeling ◽  
Multi Scale Modeling

Synaptic memory mechanisms: Alzheimer's disease amyloid β-peptide-induced dysfunction

2007 ◽  
Vol 35 (5) ◽  
pp. 1219-1223 ◽  
Author(s):  
M.J. Rowan ◽  
I. Klyubin ◽  
Q. Wang ◽  
N.W. Hu ◽  
R. Anwyl
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Synaptic Plasticity ◽  
Nitrosative Stress ◽  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Peptide ◽  
Aβ Oligomers ◽  
Aβ Amyloid

There is growing evidence that mild cognitive impairment in early AD (Alzheimer's disease) may be due to synaptic dysfunction caused by the accumulation of non-fibrillar, oligomeric Aβ (amyloid β-peptide), long before widespread synaptic loss and neurodegeneration occurs. Soluble Aβ oligomers can rapidly disrupt synaptic memory mechanisms at extremely low concentrations via stress-activated kinases and oxidative/nitrosative stress mediators. Here, we summarize experiments that investigated whether certain putative receptors for Aβ, the αv integrin extracellular cell matrix-binding protein and the cytokine TNFα (tumour necrosis factor α) type-1 death receptor mediate Aβ oligomer-induced inhibition of LTP (long-term potentiation). Ligands that neutralize TNFα or genetic knockout of TNF-R1s (type-1 TNFα receptors) prevented Aβ-triggered inhibition of LTP in hippocampal slices. Similarly, antibodies to αv-containing integrins abrogated LTP block by Aβ. Protection against the synaptic plasticity-disruptive effects of soluble Aβ was also achieved using systemically administered small molecules targeting these mechanisms in vivo. Taken together, this research lends support to therapeutic trials of drugs antagonizing synaptic plasticity-disrupting actions of Aβ oligomers in preclinical AD.

scholarly journals Amyloid-β as a Modulator of Synaptic Plasticity

2010 ◽  
Vol 22 (3) ◽  
pp. 741-763 ◽  
Author(s):  
Mordhwaj S. Parihar ◽  
Gregory J. Brewer
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β

Non-selective NSAIDs improve the amyloid-β-mediated suppression of memory and synaptic plasticity

2015 ◽  
Vol 132 ◽  
pp. 33-41 ◽  
Author(s):  
Jafar Doost Mohammadpour ◽  
Narges Hosseinmardi ◽  
Mahyar Janahmadi ◽  
Yaghoub Fathollahi ◽  
Fereshteh Motamedi ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β

scholarly journals Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

2008 ◽  
Vol 14 (8) ◽  
pp. 837-842 ◽  
Author(s):  
Ganesh M Shankar ◽  
Shaomin Li ◽  
Tapan H Mehta ◽  
Amaya Garcia-Munoz ◽  
Nina E Shepardson ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Protein Dimers ◽  
Β Protein
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