ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
A null mutation for the alpha3 nicotinic acetylcholine (ACh) receptor gene abolishes fast synaptic activity in sympathetic ganglia and reveals that ACh output from developing preganglionic terminals is regulated in an activity-dependent retrograde manner.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Acetylcholine in Brain-Body Communication: Biological Mechanisms and Physiological Roles.International journal of molecular sciences · 2026Review
- Optimization of an autaptic culture system for studying cholinergic synapses in sympathetic ganglia.Pflugers Archiv : European journal of physiology · 2025Article
- The many enigmas of nicotine.Advances in pharmacology (San Diego, Calif.) · 2024Review
- Coffee and cigarettes: Modulation of high and low sensitivity α4β2 nicotinic acetylcholine receptors by n-MP, a biomarker of coffee consumption.Neuropharmacology · 2022Article
- An Inside Job: Molecular Determinants for Postsynaptic Localization of Nicotinic Acetylcholine Receptors.Molecules (Basel, Switzerland) · 2021Review
- α3* Nicotinic Acetylcholine Receptors in the Habenula-Interpeduncular Nucleus Circuit Regulate Nicotine Intake.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- The role of the nAChR subunits α5, β2, and β4 on synaptic transmission in the mouse superior cervical ganglion.Physiological reports · 2019Article
- α-Conotoxins active at α3-containing nicotinic acetylcholine receptors and their molecular determinants for selective inhibition.British journal of pharmacology · 2018Review
- Removing 4E-BP Enables Synapses to Refine without Postsynaptic Activity.Cell reports · 2018Article
- Synapses on sympathetic neurons and parasympathetic neurons differ in their vulnerability to diabetes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Terminally differentiated epithelial cells of the thymic medulla and skin express nicotinic acetylcholine receptor subunit α 3.BioMed research international · 2014Article
- Choline transporter hemizygosity results in diminished basal extracellular dopamine levels in nucleus accumbens and blunts dopamine elevations following cocaine or nicotine.Biochemical pharmacology · 2013Article
- Reactive oxygen species inactivate neuronal nicotinic acetylcholine receptors through a highly conserved cysteine near the intracellular mouth of the channel: implications for diseases that involve oxidative stress.The Journal of physiology · 2012Review
- α4β2 nicotinic acetylcholine receptors in the early postnatal mouse superior cervical ganglion.Developmental neurobiology · 2011Article
- Biochemical and functional properties of distinct nicotinic acetylcholine receptors in the superior cervical ganglion of mice with targeted deletions of nAChR subunit genes.The European journal of neuroscience · 2010Article
- PACAP/PAC1R signaling modulates acetylcholine release at neuronal nicotinic synapses.Molecular and cellular neurosciences · 2010Article
- Engineering neuronal nicotinic acetylcholine receptors with functional sensitivity to alpha-bungarotoxin: a novel alpha3-knock-in mouse.The European journal of neuroscience · 2009Article
- Cellular events in nicotine addiction.Seminars in cell & developmental biology · 2009Review
- Pituitary adenylate cyclase-activating polypeptide (PACAP) alters parasympathetic neuron gene expression in a time-dependent fashion.Journal of molecular neuroscience : MN · 2008Article
- Mitochondrial reactive oxygen species inactivate neuronal nicotinic acetylcholine receptors and induce long-term depression of fast nicotinic synaptic transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In vertebrates, synaptic activity exerts an important influence on the formation of neural circuits, yet our understanding of its role in directing presynaptic and postsynaptic differentiation during synaptogenesis is incomplete. This study investigates how activity influences synaptic differentiation as synapses mature during early postnatal life. Specifically, we ask what happens to presynaptic terminals when synapses develop without functional postsynaptic receptors and without fast synaptic transmission. To address this issue, we investigated cholinergic nicotinic synapses in sympathetic ganglia of mice with a null mutation for the alpha3 nicotinic ACh receptor gene. Disrupting the alpha3 gene completely eliminates fast excitatory synaptic potentials on postganglionic sympathetic neurons, establishing a crucial role for alpha3-containing postsynaptic receptors in synaptic transmission. Interestingly, the preganglionic nerve terminals form morphologically normal synapses with sympathetic neurons, and these synapses persist without activity in postnatal animals. Surprisingly, when stimulating the preganglionic nerve at physiological rates, we discovered a significant decrease in ACh output from the presynaptic terminals in these alpha3(-/-) sympathetic ganglia. We show that this decrease in ACh output from the presynaptic terminals results, in part, from a lack of functional high-affinity choline transporters. We conclude the following: (1) fast synaptic transmission in mammalian SCG requires alpha3 expression; (2) in the absence of activity, the preganglionic nerve forms synapses that appear morphologically normal and persist for several weeks; and (3) to sustain transmitter release, developing presynaptic terminals require an activity-dependent retrograde signal.
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