ArticleJournal of neurophysiology2013
Nicotinic receptors modulate olfactory bulb external tufted cells via an excitation-dependent inhibitory mechanism.
Article in Journal of neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 28 citations in OpenAlex.
- Coherent olfactory bulb gamma oscillations arise from coupling independent columnar oscillators.Journal of neurophysiology · 2024Article
- Circuit formation and sensory perception in the mouse olfactory system.Frontiers in neural circuits · 2024Review
- The SARS-CoV-2 Virus and the Cholinergic System: Spike Protein Interaction with Human Nicotinic Acetylcholine Receptors and the Nicotinic Agonist Varenicline.International journal of molecular sciences · 2023Article
- Modulation of Neural Microcircuits That Control Complex Dynamics in Olfactory Networks.Frontiers in cellular neuroscience · 2021Article
- Extrinsic neuromodulation in the rodent olfactory bulb.Cell and tissue research · 2021Review
- Input dependent modulation of olfactory bulb activity by HDB GABAergic projections.Scientific reports · 2020Article
- Effects of nicotine on odor-induced increases in regional blood flow in the olfactory bulb in rats.The journal of physiological sciences : JPS · 2019Article
- A dominant role for the beta 4 nicotinic receptor subunit in nicotinic modulation of glomerular microcircuits in the mouse olfactory bulb.Journal of neurophysiology · 2018Article
- Olfactory Dysfunction in Neurodegenerative Diseases.Current allergy and asthma reports · 2018Review
- Layer- and cell type-selective co-transmission by a basal forebrain cholinergic projection to the olfactory bulb.Nature communications · 2017Article
- Mice Lacking M1 and M3 Muscarinic Acetylcholine Receptors Have Impaired Odor Discrimination and Learning.Frontiers in synaptic neuroscience · 2017Article
- Activation of β-noradrenergic receptors enhances rhythmic bursting in mouse olfactory bulb external tufted cells.Journal of neurophysiology · 2016Article
- Increased olfactory bulb acetylcholine bi-directionally modulates glomerular odor sensitivity.Scientific reports · 2016Article
- Serotonin increases synaptic activity in olfactory bulb glomeruli.Journal of neurophysiology · 2016Article
- Internal Cholinergic Regulation of Learning and Recall in a Model of Olfactory Processing.Frontiers in cellular neuroscience · 2016Article
- Functional differentiation of cholinergic and noradrenergic modulation in a biophysical model of olfactory bulb granule cells.Journal of neurophysiology · 2015Article
- Differential Muscarinic Modulation in the Olfactory Bulb.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Signaling between periglomerular cells reveals a bimodal role for GABA in modulating glomerular microcircuitry in the olfactory bulb.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Muscarinic receptors modulate dendrodendritic inhibitory synapses to sculpt glomerular output.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Synaptic connectivity of the cholinergic axons in the olfactory bulb of the cynomolgus monkey.Frontiers in neuroanatomy · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Olfactory bulb (OB) glomeruli, the initial sites of synaptic processing of odor information, exhibit high levels of nicotinic acetylcholine receptor (nAChR) expression and receive strong cholinergic input from the basal forebrain. The role of glomerular nAChRs in olfactory processing, however, remains to be elucidated. External tufted (ET) cells are a major source of excitation in the glomerulus and an important component of OB physiology. We have examined the role of nAChRs in modulating ET cell activity using whole-cell electrophysiology in mouse OB slices. We show here that the activation of glomerular nAChRs leads to direct ET cell excitation, as well as an increase in the frequency of spontaneous postsynaptic GABAergic currents. β2-containing nAChRs, likely the α4β2*-nAChR subtype (* represents the possible presence of other subunits), were significant contributors to these effects. The nAChR-mediated increase in spontaneous postsynaptic GABAergic current frequency on ET cells was, for the most part, dependent on glutamate receptor activation, thus implicating a role for excitation-dependent inhibition within the glomerulus. β2-containing nAChRs also regulate the frequency of miniature inhibitory postsynaptic currents on ET cells, implying nicotinic modulation of dendrodendritic signaling between ET and periglomerular cells. Our data also indicate that nAChR activation does not affect spontaneous or evoked transmission at the olfactory nerve-to-ET cell synapse. The results from this study suggest that ET cells, along with mitral cells, play an important role in the nicotinic modulation of glomerular inhibition.
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