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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
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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
This database was supported by the Human Brain Project (NIDCD, NIMH, NIA, NICD, NINDS) and MURI (Multidisciplinary University Research Initiative). It is now supported by RO1 DC 009977 from the National Institute for Deafness and other Communication Disorders.
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