Pathological mechanism

Data

Name BACE1 required for LTP at mossy fiber-CA3 synapses

Description

Hypothesis Abeta Physiological effect Show Other

Extracelular pathological element

Intracelular pathological element BACE1 (beta-secretase) Show Other

Pathological action Is Required For Show Other

Process LTP Show Other

Process action

Transmitter(s)

Receptor(s)

Channel(s)

Pharmacological Agent Calcium (extracellular) Show Other

Pharmacological Action Reverses Show Other

Brain region Hippocampus CA1 Show Other

Neuron Hippocampus CA3 pyramidal GLU cell Show Other

Cell model Brain slice preparations Show Other

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 Show Other

Stage Early Show Other

Question

Claim