ArticleFrontiers in behavioral neuroscience2019
Olfactory Bulb Muscarinic Acetylcholine Type 1 Receptors Are Required for Acquisition of Olfactory Fear Learning.
Article in Frontiers in behavioral neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Basal forebrain cholinergic input mediates adaptive attention allocation to enhance olfactory discrimination.PLoS biology · 2025Article
- Epigenetic rewiring of pathways related to odour perception in immune cells exposed to SARS-CoV-2Epigenetics · 2022Article
- Article
- The Response Dynamics and Function of Cholinergic and GABAergic Neurons in the Basal Forebrain During Olfactory Learning.Frontiers in cellular neuroscience · 2022Article
- Top-down acetylcholine signaling via olfactory bulb vasopressin cells contributes to social discrimination in rats.Communications biology · 2021Article
- Extrinsic neuromodulation in the rodent olfactory bulb.Cell and tissue research · 2021Review
- Modulation of Neural Microcircuits That Control Complex Dynamics in Olfactory Networks.Frontiers in cellular neuroscience · 2021Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The olfactory bulb (OB) receives significant cholinergic innervation and widely expresses cholinergic receptors. While acetylcholine (ACh) is essential for olfactory learning, the exact mechanisms by which ACh modulates olfactory learning and whether it is specifically required in the OB remains unknown. Using behavioral pharmacology and optogenetics, we investigated the role of OB ACh in a simple olfactory fear learning paradigm. We find that antagonizing muscarinic ACh receptors (mAChRs) in the OB during fear conditioning but not testing significantly reduces freezing to the conditioned odor, without altering olfactory abilities. Additionally, we demonstrate that m1 mAChRs, rather than m2, are required for acquisition of olfactory fear. Finally, using mice expressing channelrhodopsin in cholinergic neurons, we show that stimulating ACh release specifically in the OB during odor-shock pairing can strengthen olfactory fear learning. Together these results define a role for ACh in olfactory associative learning and OB glomerular plasticity.
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