Oligomeric amyloid-β peptide disrupts olfactory information output by impairment of local inhibitory circuits in rat olfactory bulb
Abstract
Although early olfactory dysfunction has been found in patients with Alzheimer's disease, the underlying mechanisms remain unclear. In this study, we investigated whether and how oligomeric amyloid-β peptide (Aβ) affects the responses of mitral cells (MCs). We found that oligomeric Aβ1-42 increased spontaneous and evoked firing rates but decreased the ratio of evoked to spontaneous firings in MCs. Aβ1-42 oligomers showed no impact on the hyperactivity exerted by pharmacological blockage of GABA A receptors, suggesting an involvement of GABAergic inhibitory transmission in Aβ1 to 42-induced over-excitability. It was further determined that Aβ1-42 oligomers inhibited the frequency of spontaneous inhibitory postsynaptic currents and miniature inhibitory postsynaptic currents, as well as the amplitude of miniature inhibitory postsynaptic currents in MCs. Both recurrent and lateral inhibition of MCs, which are critical for odor discrimination, were also disrupted by Aβ1-42 oligomers. The above data indicate that Aβ impairs local inhibitory circuits and thereby leads to perturbations of olfactory information output in the olfactory bulb. This study reveals a cellular and synaptic basis of olfactory deficits associated with Alzheimer's disease.
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Evidence suggests disrupted GABA signaling in the olfactory bulb may mediate olfactory loss in Alzheimer's disease.
“and evidence suggests disrupted GABA signaling in the olfactory bulb may mediate this olfactory loss [147].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [147]
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Self-citation
- Authors
- Hu, B., Geng, C., & Hou, X.-Y.
- Affiliations
- Xuzhou Medical College (CN)
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2017-03
- Volume
- 51
- Pages
- 113-121
- ISSN
- 0197-4580 (ISSN-L)
- OpenAlex
- W2566881733
- Cited by
- 34
- References
- 41
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 7 · 2023: 1 · 2022: 1 · 2021: 8 · 2020: 7 · 2019: 4 · 2018: 2 · 2017: 1
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81473185)
- Jiangsu Qinglan Project for Innovative Teams
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Sensory Systems › Olfactory and Sensory Function Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- amyloid-beta oligomers, amyloid-beta 42, olfactory bulb, mitral cells, olfactory dysfunction, Alzheimer's disease, GABAergic inhibition, inhibitory postsynaptic currents, miniature inhibitory postsynaptic currents, recurrent inhibition, lateral inhibition, odor discrimination, neuronal excitability
- MeSH terms
- Alzheimer Disease, Animals, Olfaction Disorders, gamma-Aminobutyric Acid, Olfactory Bulb, Peptide Fragments, Smell, Amyloid beta-Peptides, Rats, Sprague-Dawley, Inhibitory Postsynaptic Potentials
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