ArticleThe Journal of physiology1997
Stimulation of a nicotinic ACh receptor causes depolarization and activation of L-type Ca2+ channels in rat pinealocytes.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 60 citations in OpenAlex.
- Bidirectional Modulation of Beam Traversal Performance by Acetylcholine in the Cerebellar Nuclei.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Further Insights Into Anticholinergic Action Informed by Japanese Anticholinergic Risk Scale.Geriatrics & gerontology international · 2026Review
- Mass-spectrometry analysis of the human pineal proteome during night and day and in autism.Journal of pineal research · 2021Article
- TMEM16A and TMEM16B channel proteins generate CaThe Journal of biological chemistry · 2018Article
- Modulation of Ca2+ oscillation and melatonin secretion by BKCa channel activity in rat pinealocytes.American journal of physiology. Cell physiology · 2016Article
- Noradrenaline upregulates T-type calcium channels in rat pinealocytes.The Journal of physiology · 2015Article
- Modulation of nicotinic receptor channels by adrenergic stimulation in rat pinealocytes.American journal of physiology. Cell physiology · 2014Article
- Developmental and diurnal expression of the synaptosomal-associated protein 25 (Snap25) in the rat pineal gland.Neurochemical research · 2013Article
- Norepinephrine causes a biphasic change in mammalian pinealocye membrane potential: role of alpha1B-adrenoreceptors, phospholipase C, and Ca2+.Endocrinology · 2011Article
- Glutamate transporter-mediated glutamate secretion in the mammalian pineal gland.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- It is not "either/or": activation and desensitization of nicotinic acetylcholine receptors both contribute to behaviors related to nicotine addiction and mood.Progress in neurobiology · 2008Review
- Review
- A CACNA1F mutation identified in an X-linked retinal disorder shifts the voltage dependence of Cav1.4 channel activation.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Acetylcholine triggers L-glutamate exocytosis via nicotinic receptors and inhibits melatonin synthesis in rat pinealocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Signal transduction molecules in the rat pineal organ: Ca2+, pCREB, and ICER.Die Naturwissenschaften · 1996Review
- Cholinoreceptors of early (preneural) sea urchin embryos.Neuroscience and behavioral physiologyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Membrane voltage (Vm) recordings were obtained from isolated rat pinealocytes using the patch-clamp technique. In parallel to the electrophysiological experiments, intracellular Ca2+ measurements were performed using fura-2. 2. The resting Vm averaged -43 mV and replacement of extracellular NaCl by KCl completely depolarized the cells. This indicates that the resting Vm is dominated by a K+ conductance. Single-channel recordings revealed the presence of a large conductance Ca(2+)-activated charybdotoxin-sensitive K+ channel. 3. Application of ACh (100 microM) depolarized the pinealocytes on average by 16 mV. The depolarizing effect of ACh was mimicked by nicotine (50 microM) and was prevented by tubocurarine (100 microM). 4. The ACh-induced depolarization was largely abolished in the absence of extracellular Na+, but was not significantly affected by extracellular Ca2+ removal. 5. Application of ACh (100 microM) caused an increase in [Ca2+]i. This increase was completely dependent on the presence of extracellular Ca2+ and was largely reduced after extracellular Na+ removal. Nifedipine (1 microM) reduced the ACh-induced increase in [Ca2+]i by about 50%. 6. Our findings indicate that in rat pinealocytes stimulation of a nicotinic ACh receptor (nAChR) induces depolarization mainly by Na+ influx via the nAChR. The depolarization then activates L-type Ca2+ channels, which are responsible for the nifedipine-sensitive portion of the intracellular Ca2+ increase. Ca2+ influx via the nAChR probably also contributes to the observed rise in [Ca2+]i.
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