BACE1 Is Necessary for Experience-Dependent Homeostatic Synaptic Plasticity in Visual Cortex
Open accessAbstract
Alzheimer’s disease (AD) is the most common form of age-related dementia, which is thought to result from overproduction and/or reduced clearance of amyloid-beta (A β) peptides. Studies over the past few decades suggest that A β is produced in an activity-dependent manner and has physiological relevance to normal brain functions. Similarly, physiological functions for β- and γ-secretases, the two key enzymes that produce A β by sequentially processing the amyloid precursor protein (APP), have been discovered over recent years. In particular, activity-dependent production of A β has been suggested to play a role in homeostatic regulation of excitatory synaptic function. There is accumulating evidence that activity-dependent immediate early gene Arc is an activity “sensor,” which acts upstream of A β production and triggers AMPA receptor endocytosis to homeostatically downregulate the strength of excitatory synaptic transmission. We previously reported that Arc is critical for sensory experience-dependent homeostatic reduction of excitatory synaptic transmission in the superficial layers of visual cortex. Here we demonstrate that mice lacking the major neuronal β-secretase, BACE1, exhibit a similar phenotype: stronger basal excitatory synaptic transmission and failure to adapt to changes in visual experience. Our results indicate that BACE1 plays an essential role in sensory experience-dependent homeostatic synaptic plasticity in the neocortex.
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Complete loss of Bace1 in mice leads to schizophrenia-like phenotypes and deficits in cognitive function, mossy fiber long-term potentiation (LTP), synaptic plasticity, and axon guidance.
“Complete loss of Bace1 in mice are known to lead to schizophrenia-like phenotypes and deficits in cognitive function, mossy fiber long-term potentiation (LTP), synaptic plasticity, and axon guidance (Savonenko et al. 2008, Wang et al. 2008a, Petrus & Lee 2014, Hitt et al. 2012, Rajapaksha et al. 2011).”
From miR‐186 is decreased in aged brain and suppresses <scp>BACE</scp>1 expression (2016) · cites this paper as Petrus & Lee 2014
The Results and Discussion (page unavailable) report that BACE1 knockout mice lack experience-dependent homeostatic synaptic plasticity in visual cortex, supporting the synaptic-plasticity part of the sentence. Our copy does not report schizophrenia-like phenotypes, cognitive deficits, mossy fiber LTP deficits, or axon-guidance deficits in these mice; it mentions axon myelination, which is different from guidance. (LLM, conf=0.86)
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- Authors
- Petrus, E., & Lee, H.-K.
- Affiliations
- Johns Hopkins University (US)
- Corresponding author
- Lee, Hey-Kyoung
- Venue
- Neural Plasticity
- Publisher
- Wiley
- Published
- 2014
- Volume
- 2014
- Pages
- 1-7
- ISSN
- 1687-5443 (ISSN-L)
- 2090-5904
- PMC
- PMC4053288
- OpenAlex
- W2108132806
- Cited by
- 19
- References
- 58
- Citations by year
- 2026: 1 · 2022: 1 · 2021: 3 · 2020: 3 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 1 · 2015: 5 · 2014: 1
- FWCI
- 1.22
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Neural Plasticity (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Eye Institute (R01EY014882)
- National Institute of Neurological Disorders and Stroke (F31NS079058)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- BACE1, beta-secretase, homeostatic plasticity, visual cortex, excitatory synaptic transmission, amyloid-beta, Arc, AMPA receptor endocytosis, Alzheimer's disease, neocortex
- MeSH terms
- Animals, Cytoskeletal Proteins, Data Interpretation, Statistical, Homeostasis, Male, Nerve Tissue Proteins, Synaptic Transmission, Neuronal Plasticity, Visual Cortex, Aspartic Acid Endopeptidases, Pyramidal Cells, Mice, Knockout, Excitatory Postsynaptic Potentials, Mice, Amyloid Precursor Protein Secretases
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