ArticleThe Journal of physiology2000
The role of Ca2+ stores in the muscarinic inhibition of the K+ current IK(SO) in neonatal rat cerebellar granule cells.
Article in The Journal of physiology, 2000. 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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16 citing papers in PubMed, 38 citations in OpenAlex.
- Cholinergic modulation of upper airway control: maturational changes and mechanisms at cellular and synaptic levels.Journal of neurophysiology · 2025Review
- The role of two-pore-domain background K⁺ (K₂p) channels in the thalamus.Pflugers Archiv : European journal of physiology · 2015Review
- The cellular building blocks of breathing.Comprehensive Physiology · 2012Review
- Identification of the muscarinic pathway underlying cessation of sleep-related burst activity in rat thalamocortical relay neurons.Pflugers Archiv : European journal of physiology · 2012Article
- Probing the regulation of TASK potassium channels by PI4,5P₂ with switchable phosphoinositide phosphatases.The Journal of physiology · 2011Article
- Modulation of GABAergic transmission by muscarinic receptors in the entorhinal cortex of juvenile rats.Journal of neurophysiology · 2009Article
- Calcium-independent phospholipase A2 mediates store-operated calcium entry in rat cerebellar granule cells.Cerebellum (London, England) · 2008Article
- Neuronal two-pore-domain potassium channels and their regulation by G protein-coupled receptors.The Journal of physiology · 2007Review
- Inhibition of a background potassium channel by Gq protein alpha-subunits.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Properties and modulation of the G protein-coupled K+ channel in rat cerebellar granule neurons: ATP versus phosphatidylinositol 4,5-bisphosphate.The Journal of physiology · 2003Article
- What are the roles of the many different types of potassium channel expressed in cerebellar granule cells?Cerebellum (London, England) · 2003Review
- Hipnic modulation of cerebellar information processing: implications for the cerebro-cerebellar dialogue.Cerebellum (London, England) · 2003Review
- Characterization of four types of background potassium channels in rat cerebellar granule neurons.The Journal of physiology · 2002Article
- Acute synaptic modulation by nicotinic agonists in developing cerebellar Purkinje cells of the rat.The Journal of physiology · 2002Article
- Group I metabotropic glutamate receptors elicit epileptiform discharges in the hippocampus through PLCbeta1 signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Deafness associated changes in expression of two-pore domain potassium channels in the rat cochlear nucleus.Hearing researchArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebellar granule neurons (CGNs) possess a standing outward potassium current (IK(SO)) which shares many similarities with current through the two-pore domain potassium channel TASK-1 and which is inhibited following activation of muscarinic acetylcholine receptors. The action of muscarine on IK(SO) was unaffected by the M2 receptor antagonist methoctramine (100 nM) but was blocked by the M3 antagonist zamifenacin, which, at a concentration of 100 nM, shifted the muscarine concentration-response curve to the right by around 50-fold. Surprisingly, M3 receptor activation rarely produced a detectable increase in [Ca2+]i unless preceded by depolarization of the cells with 25 mM K+. Experiments with thapsigargin and ionomycin suggested that the endoplasmic reticulum Ca2+ stores in CGNs were depleted at rest. In contrast, cerebellar glial cells in the same fields of cells possessed substantial endoplasmic reticulum Ca2+ stores at rest. Pretreatment of the cells with BAPTA AM, thapsigargin or the phospholipase C (PLC) inhibitor U-73122 all blocked the muscarine-induced Ca2+ signal but had little or no effect on muscarinic inhibition of IK(SO). Raising [Ca2+]i directly with ionomycin caused a small but significant inhibition of IK(SO). It is concluded that muscarine acts on M3 muscarinic acetylcholine receptors both to inhibit IK(SO) and to mobilize Ca2+ from intracellular stores in CGNs. While the mobilization of Ca2+ occurs through activation of PLC, this does not seem to be the primary mechanism underlying muscarinic inhibition of IK(SO).
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