Glutamatergic Contributions to Nicotinic Acetylcholine Receptor Agonist-Evoked Cholinergic Transients in the Prefrontal Cortex
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Because modulation of cortical cholinergic neurotransmission has been hypothesized to represent a necessary mechanism mediating the beneficial cognitive effects of nicotine and nicotinic acetylcholine receptor (nAChR) subtype-selective agonists, we used choline-sensitive microelectrodes for the real-time measurement of ACh release in vivo, to characterize cholinergic transients evoked by nicotine and the α4β2*-selective nAChR partial agonist 2-methyl-3-(2-(S)-pyrrolindinylmethoxy)pyridine dihydrochloride (ABT-089), a clinically effective cognition enhancer. In terms of cholinergic signal amplitudes, ABT-089 was significantly more potent than nicotine in evoking ACh cholinergic transients. Moreover, cholinergic signals evoked by ABT-089 were characterized by faster signal rise time and decay rate. The nAChR antagonist mecamylamine attenuated the cholinergic signals evoked by either compound. Cholinergic signals evoked by ABT-089 were more efficaciously attenuated by the relatively β2*-selective nAChR antagonist dihydro-β-erythroidine. The α7 antagonist methyllycaconitine did not affect choline signal amplitudes but partly attenuated the relatively slow decay rate of nicotine-evoked cholinergic signals. Furthermore, the AMPA receptor antagonist DNQX as well as the NMDA receptor antagonist APV more potently attenuated cholinergic signals evoked by ABT-089. Using glutamate-sensitive microelectrodes to measure glutamatergic transients, ABT-089 was more potent than nicotine in evoking glutamate release. Glutamatergic signals were highly sensitive to tetrodotoxin-induced blockade of voltage-regulated sodium channels. Together, the present evidence indicates that compared with nicotine, ABT-089 evokes more potent and sharper cholinergic transients in prefrontal cortex. Glutamatergic mechanisms necessarily mediate the cholinergic effects of nAChR agonists in the prefrontal cortex.
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Rapid acetylcholine transients in the mPFC are correlated with attention to brief cues.
“rapid acetylcholine transients in the mPFC are correlated with attention to brief cues”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Parikh et al. 2008
Mice lacking the β2, but not the α7, subunit show impaired performance in an attentional task.
“mice lacking the β2, but not the α7, subunit show impaired performance in an attentional task (Parikh et al. 2007(Parikh et al. , 2008)).”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Parikh et al. 2008
The Subjects section describes experiments in rats, not mice lacking receptor subunits. The Discussion mentions that an α7-selective antagonist did not impair attentional performance, but does not report the claimed comparison between β2- and α7-deficient mice. Searches for knockout mice and the two subunits found no passage establishing that comparison; page numbers were unavailable in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredNicotine can stimulate the firing of both POMC neurons that signal satiety and neuropeptide Y (NPY) neurons that stimulate food seeking.
“nicotine can stimulate the firing of both POMC neurons that signal satiety, and neuropeptide Y (NPY) neurons that stimulate food seeking (Parikh et al. 2007(Parikh et al. , 2008)).”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Parikh et al. 2008
The Discussion describes nicotine-evoked neurotransmitter activity in the prefrontal cortex, not firing of POMC or NPY neurons. Searches for POMC, NPY, satiety, food seeking, and hypothalamic feeding found no passage in our copy addressing the attributed claim. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIn a slice preparation, the effects of nicotine on firing of POMC neurons persist longer than firing of NPY neurons.
“in a slice preparation, the effects of nicotine on firing of POMC neurons persist longer than firing of NPY neurons (Parikh et al. 2007(Parikh et al. , 2008))”
From Mechanisms of Nicotine Addiction (2021) · cites this paper as Parikh et al. 2008
The Methods describe in vivo recordings of cholinergic signals in the medial prefrontal cortex, and the Discussion compares the decay of nicotine- and ABT-089-evoked signals. Searches for POMC, NPY, and slice-based neuronal firing found no passage comparing nicotine’s effects on those neurons. (LLM, conf=0.78)
Experimental — accuracy not yet measured
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Self-citation
- Authors
- Parikh, V., Man, K., Decker, M. W., & Sarter, M.
- Affiliations
- University of Michigan (US)
- Abbott (United States) (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-04-02
- Volume
- 28
- Issue
- 14
- Pages
- 3769-3780
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6671097
- OpenAlex
- W2039986616
- Cited by
- 127
- References
- 71
- Citations by year
- 2025: 3 · 2024: 4 · 2023: 2 · 2022: 1 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 3 · 2017: 7 · 2016: 11 · 2015: 5 · 2014: 14 · 2013: 13 · 2012: 11
- FWCI
- 5.22
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Abbott Laboratories
- National Institute of Mental Health (R01MH080332, MH 080332)
- 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
- nicotinic acetylcholine receptors, nicotine, prefrontal cortex, glutamate release, choline release, alpha4beta2 nAChR, alpha7 nAChR, mecamylamine, dihydro-beta-erythroidine, methyllycaconitine, AMPA receptors, NMDA receptor, cognitive enhancement
- MeSH terms
- Acetylcholine, Analysis of Variance, Animals, Choline, Dihydro-beta-Erythroidine, Dose-Response Relationship, Drug, Electrochemistry, Evoked Potentials, Male, Mecamylamine, Neostigmine, Nicotine, Pyridines, Pyrrolidines, Quinoxalines, Tetrodotoxin, Valine, Prefrontal Cortex, Excitatory Amino Acid Antagonists, Glutamic Acid, Nicotinic Agonists, Nicotinic Antagonists, Sodium Channel Blockers, Rats, In Vitro Techniques
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