ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Induction of dendritic spines by β2-containing nicotinic receptors.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 69 citations in OpenAlex.
- Serotonergic modulation of excitatory synapse development and plasticity.Molecules and cells · 2026Review
- Mesoscopic analysis of GABAergic marker expression in acetylcholine neurons in the whole mouse brain.iScience · 2026Article
- Mesoscopic analysis of GABAergic marker expression in acetylcholine neurons in the whole mouse brain.bioRxiv : the preprint server for biology · 2025Article
- Activity-dependent development of synaptic circuits mediates direction selectivity in an axis-specific manner.Cell reports · 2025Article
- Water-Soluble Lynx1 Upregulates Dendritic Spine Density and Stimulates Astrocytic Network and Signaling.Molecular neurobiology · 2025Article
- Targeting high-affinity nicotinic receptors protects against the functional consequences of β-amyloid in mouse hippocampus.Molecular psychiatry · 2025Article
- Linking altered neuronal and synaptic properties to nicotinic receptor Alpha5 subunit gene dysfunction: a translational investigation in rat mPFC and human cortical layer 6.Translational psychiatry · 2025Article
- Acetylcholine Neurons Become Cholinergic during Three Time Windows in the Developing Mouse Brain.eNeuro · 2024Article
- Article
- Interactions between the Nicotinic and Endocannabinoid Receptors at the Plasma Membrane.Membranes · 2022Review
- Loss of GABA co-transmission from cholinergic neurons impairs behaviors related to hippocampal, striatal, and medial prefrontal cortex functions.Frontiers in behavioral neuroscience · 2022Article
- Review
- Nanoscale Sub-Compartmentalization of the Dendritic Spine Compartment.Biomolecules · 2021Review
- Homomeric and Heteromeric α7 Nicotinic Acetylcholine Receptors in Health and Some Central Nervous System Diseases.Membranes · 2021Review
- Dysregulation of Neuronal Nicotinic Acetylcholine Receptor-Cholesterol Crosstalk in Autism Spectrum Disorder.Frontiers in molecular neuroscience · 2021Article
- Nicotinic Receptors in Sleep-Related Hypermotor Epilepsy: Pathophysiology and Pharmacology.Brain sciences · 2020Review
- Dual recombinase fate mapping reveals a transient cholinergic phenotype in multiple populations of developing glutamatergic neurons.The Journal of comparative neurology · 2020Article
- Selective Expression of Nicotinic Receptor Sub-unit mRNA in Early Human Fetal Forebrain.Frontiers in molecular neuroscience · 2020Article
- Genetic Deletion of GABAFrontiers in cellular neuroscience · 2019Article
- [β2-nicotinic acetylcholine receptor promotes development of GABANan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Glutamatergic synapses are located mostly on dendritic spines in the adult nervous system. The spines serve as postsynaptic compartments, containing components that mediate and control the synaptic signal. Early in development, when glutamatergic synapses are initially forming, waves of excitatory activity pass through many parts of the nervous system and are driven in part by a class of heteropentameric β2-containing nicotinic acetylcholine receptors (β2*-nAChRs). These β2*-nAChRs are widely distributed and, when activated, can depolarize the membrane and elevate intracellular calcium levels in neurons. We show here that β2*-nAChRs are essential for acquisition of normal numbers of dendritic spines during development. Mice constitutively lacking the β2-nAChR gene have fewer dendritic spines than do age-matched wild-type mice at all times examined. Activation of β2*-nAChRs by nicotine either in vivo or in organotypic slice culture quickly elevates the number of spines. RNA interference studies both in vivo and in organotypic culture demonstrate that the β2*-nAChRs act in a cell-autonomous manner to increase the number of spines. The increase depends on intracellular calcium and activation of calcium, calmodulin-dependent protein kinase II. Absence of β2*-nAChRs in vivo causes a disproportionate number of glutamatergic synapses to be localized on dendritic shafts, rather than on spines as occurs in wild type. This shift in synapse location is found both in the hippocampus and cortex, indicating the breadth of the effect. Because spine synapses differ from shaft synapses in their signaling capabilities, the shift observed is likely to have significant consequences for network function.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.