ArticlePflugers Archiv : European journal of physiology2006
An alpha3beta4 subunit combination acts as a major functional nicotinic acetylcholine receptor in male rat pelvic ganglion neurons.
Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 33 citations in OpenAlex.
- Dissection of Pelvic Autonomic Ganglia and Associated Nerves in Male and Female Rats.Journal of visualized experiments : JoVE · 2020Article
- Impaired Expression of Neuregulin 1 and Nicotinic Acetylcholine Receptor β4 Subunit in Diverticular Disease.Frontiers in cellular neuroscience · 2019Article
- α-Conotoxins active at α3-containing nicotinic acetylcholine receptors and their molecular determinants for selective inhibition.British journal of pharmacology · 2018Review
- Intravenous Infusion of Bone Marrow-Derived Mesenchymal Stem Cells Reduces Erectile Dysfunction Following Cavernous Nerve Injury in Rats.Sexual medicine · 2018Article
- Alanine scan of α-conotoxin RegIIA reveals a selective α3β4 nicotinic acetylcholine receptor antagonist.The Journal of biological chemistry · 2015Article
- Developing a functional urinary bladder: a neuronal context.Frontiers in cell and developmental biology · 2015Review
- Decrease in neuronal nicotinic acetylcholine receptor subunit and PSD-93 transcript levels in the male mouse MPG after cavernous nerve injury or explant culture.American journal of physiology. Renal physiology · 2013Article
- Synaptic transmission at parasympathetic neurons of the major pelvic ganglion from normal and diabetic male mice.Journal of neurophysiology · 2013Article
- Cross-reactivity of acid-sensing ion channel and Na⁺-H⁺ exchanger antagonists with nicotinic acetylcholine receptors.The Journal of physiology · 2011Article
- Fast synaptic transmission in the goldfish CNS mediated by multiple nicotinic receptors.The Journal of physiology · 2011Article
- Nicotine activates TRPM5-dependent and independent taste pathways.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We identified major subunits of the nicotinic acetylcholine receptor (nAChR) involved in excitatory postsynaptic potential and intracellular Ca(2+) ([Ca(2+)]i) increase in the major pelvic ganglion (MPG) neurons of the male rat. ACh elicited fast inward currents in both sympathetic and parasympathetic MPG neurons. Mecamylamine, a selective antagonist for alpha3beta4 nAChR, potently inhibited the ACh-induced currents in sympathetic and parasympathetic neurons (IC(50); 0.53 and 0.22 microM, respectively). Furthermore, alpha-conotoxin AuIB (10 microM), a new selective antagonist for alpha3beta4 nAChR, blocked more than 80% of the ACh-induced currents in MPG neurons. Conversely, alpha-bungarotoxin, alpha-methyllycaconitine, and dihydro-beta-erythroidine, known as blockers of the alpha7 or alpha4beta2, did not show selective blocking effects on MPG neurons. ACh transiently increased [Ca(2+)]i which was subsequently abolished in the extracellular Ca(2+)-free environment. Simultaneous recording of [Ca(2+)]i and ionic currents revealed that ACh increased [Ca(2+)]i under the conditions of the voltage-clamped (at -80 mV) state, and this resulted from the influx through nAChR itself. ACh-induced [Ca(2+)]i increase was blocked by mecamylamine (10 microM), but was not affected by atropine (1 microM). RT-PCR analysis showed that, among subunits of nAChR, alpha3 and beta4 were predominantly expressed in MPG. We suggest that activation of alpha3 and beta4 nAChR subunits in MPG neurons induce fast inward currents and [Ca(2+)]i increase, possibly mediating a major role in pelvic autonomic synaptic transmission.
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.