Facilitation of glutamatergic neurotransmission by presynaptic nicotinic acetylcholine receptors
Abstract
The profiles of presynaptic facilitation of glutamate release as elicited by nicotine and acetylcholine were compared in two limbic pathways recapitulated in vitro. At synapses of medial habenula (MHN) and interpeduncular nucleus (IPN) neurons, application of nicotine increased the frequency of TTX-resistant, spontaneous postsynaptic currents (SSCs) by an average of 5-fold. In contrast, the average increase in SSC frequency elicited by nicotine was more than 120 fold at synapses of olfactory bulb (OB) and amygdala neurons. At both preparations, pulses of ACh caused presynaptic facilitation that lasted longer than that elicited by nicotine. The subunit composition of presynaptic nAChRs may contribute to the different profiles of facilitation observed. The large magnitude, fast kinetics, and alpha-bungarotoxin sensitivity of facilitation observed at OB-amygdala synapses is consistent with participation of alpha7-type nAChRs. As subunit-selective deletion of alpha5 or alpha7 altered the profile of nicotine-elicited facilitation at MHN-IPN synapses, presynaptic nAChRs at MHN-IPN synapses appear to be more complex. Such heteromeric combinations of nAChRs may contribute to the lower magnitude and slower kinetics of presynaptic facilitation at MHN-IPN synapses. Calcium influx through either voltage-gated calcium channels or directly through presynaptic alpha7-containing nAChRs is sufficient to support nicotine-elicited facilitation of glutamate release. Resultant increases in intrac…
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Most MHb neurons also produce and corelease glutamate, which is considered the major functional transmitter at the MHb-IPN synapse.
“However, it is believed that most MHb neurons also produce and corelease glutamate, with this excitatory neurotransmitter considered the major functional transmitter at the MHb-IPN synapse (Mata et al. 1977;Vincent et al. 1980;Girod et al. 2000;Ren et al., 2011).”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Girod et al. 2000
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References 55 · Cited by 122
- Authors
- Girod, R., Barazangi, N., McGehee, D., & Role, L. W.
- Affiliations
- Columbia University (US)
- Corresponding author
- Role, Lorna W
- ORCID
- Role, Lorna W
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2000-12
- Volume
- 39
- Issue
- 13
- Pages
- 2715-2725
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W2095187162
- Cited by
- 122
- References
- 55
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 3 · 2022: 1 · 2021: 3 · 2020: 3 · 2019: 1 · 2018: 5 · 2017: 1 · 2016: 1 · 2015: 8 · 2014: 5 · 2013: 6 · 2012: 6
- FWCI
- 2.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01da009366-05)
- National Institute on Drug Abuse (DA-09366, DA05840)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
- Keywords
- presynaptic nicotinic acetylcholine receptors, glutamate release, presynaptic facilitation, nicotine, acetylcholine, medial habenula, interpeduncular nucleus, olfactory bulb, amygdala, alpha7 nAChR, spontaneous postsynaptic currents, calcium influx
- MeSH terms
- Animals, Calcium, Chick Embryo, Electrophysiology, Female, Mesencephalon, Synaptic Transmission, Olfactory Bulb, Pregnancy, Receptors, Nicotinic, Synapses, Oligonucleotides, Antisense, Receptors, Presynaptic, Glutamic Acid, Habenula, Mice, alpha7 Nicotinic Acetylcholine Receptor
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