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Pathological mechanism
Name
BACE1 required for LTP at mossy fiber-CA3 synapses
Description
Hypothesis
Abeta Physiological effect
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Extracelular pathological element
Intracelular pathological element
BACE1 (beta-secretase)
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Pathological action
Is Required For
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Process
LTP
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Process action
Transmitter(s)
Receptor(s)
Channel(s)
Pharmacological Agent
Calcium (extracellular)
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Pharmacological Action
Reverses
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Brain region
Hippocampus
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Neuron
CA3 pyramidal neuron
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Cell model
Brain slice preparations
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Cellular compartment
PubMed ID
18753368
Citation
AlzWeb
Notes
BACE1 knock-out mice display reduced presynaptic function at the mossy fiber projections in CA3. Mossy fiber long-term potentiation (LTP), which is normally expressed via an increase in presynaptic release, was eliminated in the knock-outs. The specific deficit in mossy fiber LTP was upstream of cAMP signaling and could be "rescued" by transiently elevating extracellular Ca2+ concentration. These results suggest that BACE1 may play a critical role in regulating presynaptic function, especially activity-dependent strengthening of presynaptic release, at mossy fiber synapses. BACE1 knock-outs display deficits in activity-dependent potentiation of synaptic transmission at mossy fiber to CA3 synapses in the hippocampus.Wang H, Song L, Laird F, Wong PC, Lee HK. J Neurosci. 2008 Aug 27;28(35):8677-81.
Pathology
Alzheimer
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Stage
Early
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Question
Claim
Other categories referring to "
BACE1 required for LTP at mossy fiber-CA3 synapses
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Revisions:
4
Last time:
9/5/2008 12:41:16 PM
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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