ArticleBiochemical pharmacology2011
An autoradiographic survey of mouse brain nicotinic acetylcholine receptors defined by null mutants.
Article in Biochemical pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 72 citations in OpenAlex.
- An Exploratory Trial of Transdermal Nicotine for Aggression and Irritability in Adults with Autism Spectrum Disorder.Journal of autism and developmental disorders · 2018Trial
- Hedgehog-interacting protein acts in the habenula to regulate nicotine intake.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Development ofACS chemical neuroscience · 2022Article
- Adolescent nicotine administration increases nicotinic acetylcholine receptor binding and functional connectivity in specific cortico-striatal-thalamic circuits.Brain communications · 2022Article
- Effect of Intrahippocampal Administration of α7 Subtype Nicotinic Receptor Agonist PNU-282987 and Its Solvent Dimethyl Sulfoxide on the Efficiency of Hypoxic Preconditioning in Rats.Molecules (Basel, Switzerland) · 2021Article
- The Periaqueductal Gray and Its Extended Participation in Drug Addiction Phenomena.Neuroscience bulletin · 2021Review
- Article
- Partial and full deletion of nicotinic acetylcholine receptor α4 and β2 subunits reduces sensitivity to acute nicotine administration and development of tolerance following chronic nicotine administration.Behavioural pharmacology · 2020Article
- Regulation of aggressive behaviors by nicotinic acetylcholine receptors: Animal models, human genetics, and clinical studies.Neuropharmacology · 2020Review
- β4-Nicotinic Receptors Are Critically Involved in Reward-Related Behaviors and Self-Regulation of Nicotine Reinforcement.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- The α5 Nicotinic Acetylcholine Receptor Subunit Differentially Modulates α4β2Frontiers in synaptic neuroscience · 2020Review
- PeIA-5466: A Novel Peptide Antagonist Containing Non-natural Amino Acids That Selectively Targets α3β2 Nicotinic Acetylcholine Receptors.Journal of medicinal chemistry · 2019Article
- Distribution of α7 Nicotinic Acetylcholine Receptor Subunit mRNA in the Developing Mouse.Frontiers in neuroanatomy · 2019Article
- Article
- The interaction of the Chrna5 D398N variant with developmental nicotine exposure.Genes, brain, and behavior · 2018Article
- Chrna5-Expressing Neurons in the Interpeduncular Nucleus Mediate Aversion Primed by Prior Stimulation or Nicotine Exposure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Knockout of alpha 5 nicotinic acetylcholine receptors subunit alters ethanol-mediated behavioral effects and reward in mice.Neuropharmacology · 2018Article
- Differential effects of withdrawal from intermittent and continuous nicotine exposure on reward deficit and somatic aspects of nicotine withdrawal and expression of α4β2* nAChRs in Wistar male rats.Pharmacology, biochemistry, and behavior · 2018Article
- Reduced α4 subunit expression in α4British journal of pharmacology · 2018Article
- Bidirectional Regulation of Aggression in Mice by Hippocampal Alpha-7 Nicotinic Acetylcholine Receptors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Nine nicotinic receptor subunits are expressed in the central nervous system indicating that a variety of nicotinic acetylcholine receptors (nAChR) may be assembled. A useful method with which to identify putative nAChR is radioligand binding. In the current study the binding of [(125)I]α-bungarotoxin, [(125)I]α-conotoxinMII, 5[(125)I]-3-((2S)-azetidinylmethoxy)pyridine (A-85380), and [(125)I]epibatidine has been measured autoradiographically to provide data on many nAChR binding sites. Each binding site was evaluated semi-quantitatively for samples prepared from wild-type and α2, α4, α6, α7, β2, β4, α5 and β3 null mutant mice. Deletion of the α7 subunit completely and selectively eliminated [(125)I]α-bungarotoxin binding. The binding of [(125)I]α-conotoxinMII was eliminated in most brain regions by deletion of either the α6 or β2 subunit and is reduced by deletion of either the α4 or β3 subunit. The binding of 5[(125)I]A-85380 was completely eliminated by deletion of the β2 subunit and significantly reduced by deletion of the α4 subunit. Most, but not all, α4-independent sites require expression of the α6 subunit. The effect of gene deletion on total [(125)I]epibatidine binding was very similar to that on [(125)I]A-85380 binding. [(125)I]Epibatidine also labels β4* nAChR, which was readily apparent for incubations conducted in the presence of 100nM cytisine. The effects of α3 gene deletion could not be evaluated, but persistence of residual sites implies the expression of α3* nAChR. Taken together these results confirm and extend previously published evaluations of the effect of nAChR gene deletion and help to define the nAChR subtypes measurable by ligand binding.
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