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Pathological mechanism
Name
Glutamatergic synaptic depression by synthetic amyloid beta-peptide in the medial septum.
Description
Hypothesis
Extracelular pathological element
β-Amyloid
 
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Intracelular pathological element
Pathological action
Reduces
 
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Process
Glutamatergic Synapse Activity
 
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Process action
Transmitter(s)
Glutamate
 
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Receptor(s)
Muscarinic
 
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Channel(s)
I L high threshold
 
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Pharmacological Agent
Pirenzepine
 
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Atropine
 
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Calcicludine
 
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Pharmacological Action
Blocks
 
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Brain region
Neuron
Cell model
Brain slice preparations
 
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Cellular compartment
PubMed ID
17171714
Citation
AlzWeb
Notes
Glutamatergic synaptic depression by synthetic amyloid beta-peptide in the medial septum.Santos-Torres J, Fuente A, Criado JM, Riolobos AS, Heredia M, Yajeya J. BetaA effect was blocked by calcicludine (50 nM), a selective antagonist of L-type calcium channels, and also by blocking muscarinic receptors with atropine (5 muM) or pirenzepine (1 microM), a more specific M1-receptor blocker.
Pathology
Stage
Question
Claim
Other categories referring to "
Glutamatergic synaptic depression by synthetic amyloid beta-peptide in the medial septum.
"
Revisions:
3
Last time:
11/21/2008 10:47:46 AM
Reviewer:
Pradeep Mutalik
Owner:
Pradeep Mutalik
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