Journal article
Ca2+ influx in resting rat sensory neurones that regulates and is regulated by ryanodine-sensitive Ca2+ stores
The Journal of physiology, Vol.519(Pt 1), pp.115-130
08/15/1999
DOI: 10.1111/j.1469-7793.1999.0115o.x
PMCID: PMC2269497
PMID: 10432343
Abstract
Store-operated, voltage-independent Ca\n2+\nchannels are activated by depletion of intracellular Ca\n2+\nstores and mediate Ca\n2+\ninflux into non-excitable cells at resting membrane potential. We used microfluorimetry, patch-clamp and Mn\n2+\n-quench techniques to explore the possibility that a similar mechanism exists in rat dorsal root ganglion (DRG) neurones in primary culture.\nFollowing caffeine-induced depletion, ryanodine-sensitive Ca\n2+\nstores refilled with Ca\n2+\nat resting membrane potential. The refilling process required extracellular Ca\n2+\n, was blocked by 2 mM Ni\n2+\n, and was facilitated by membrane hyperpolarization from −55 to −80 mV, indicating a key role for Ca\n2+\ninflux. This influx of Ca\n2+\nwas not affected by the voltage-operated Ca\n2+\nchannel (VOCC) antagonists nicardipine (10 μM), nimodipine (10 μ\nm\n) or ω-grammotoxin SIA (1 μ\nm\n).\nWhen ryanodine-sensitive Ca\n2+\nstores were depleted in Ca\n2+\n-free media, a return to 2 mM external Ca\n2+\nresulted in a pronounced [Ca\n2+\n]\ni\novershoot, indicating an increased permeability to Ca\n2+\n. Depletion of Ca\n2+\nstores also produced a 2-fold increase in the rate of Mn\n2+\ninflux. The [Ca\n2+\n]\ni\novershoot and Mn\n2+\nentry were both inhibited by Ni\n2+\n, but not by VOCC antagonists.\nCaffeine induced periodic Ca\n2+\nrelease from, and reuptake into, ryanodine-sensitive stores. The [Ca\n2+\n]\ni\noscillations were arrested by removal of extracellular Ca\n2+\nor by addition of Ni\n2+\n, but they were not affected by VOCC antagonists. Hyperpolarization increased the frequency of this rhythmic activity.\nThese data suggest the presence of a Ca\n2+\nentry pathway in mammalian sensory neurones that is distinct from VOCCs and is regulated by ryanodine-sensitive Ca\n2+\nstores. This pathway participates in refilling intracellular Ca\n2+\nstores and maintaining [Ca\n2+\n]\ni\noscillations and thus controls the balance between intra- and extracellular Ca\n2+\nreservoirs in resting DRG neurones.
Details
- Title: Subtitle
- Ca2+ influx in resting rat sensory neurones that regulates and is regulated by ryanodine-sensitive Ca2+ stores
- Creators
- Yuriy M UsachevStanley A Thayer
- Resource Type
- Journal article
- Publication Details
- The Journal of physiology, Vol.519(Pt 1), pp.115-130
- Publisher
- Blackwell Science Inc
- DOI
- 10.1111/j.1469-7793.1999.0115o.x
- PMID
- 10432343
- PMCID
- PMC2269497
- ISSN
- 0022-3751
- eISSN
- 1469-7793
- Language
- English
- Date published
- 08/15/1999
- Academic Unit
- Iowa Neuroscience Institute; Anesthesia; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology
- Record Identifier
- 9984070412202771
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