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Ca(2+)-induced Ca2+ release and its activation in response to a single action potential in rabbit otic ganglion cells
1. Ryanodine-sensitive intracellular Ca2+ release activated by Ca2+ entry was studied with fura-2 fluorescence and intracellular voltage recording techniques in rabbit otic ganglion cells. 2. The removal of extracellular Ca2+ reduced sustained, transient or oscillatory rises in intracellular Ca2+ ([...
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Published in: | The Journal of physiology 1995-07, Vol.486 (Pt 1), p.177-187 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | 1. Ryanodine-sensitive intracellular Ca2+ release activated by Ca2+ entry was studied with fura-2 fluorescence and intracellular
voltage recording techniques in rabbit otic ganglion cells. 2. The removal of extracellular Ca2+ reduced sustained, transient
or oscillatory rises in intracellular Ca2+ ([Ca2+]i) induced at high extracellular K+ and abolished the [Ca2+]i oscillation
in cultured neurones. 3. Ryanodine (10 microM) transiently increased [Ca2+]i and reduced the amplitude and rate of rise of
the high-K(+)-induced rise in [Ca2+]i, while caffeine (5 mM) produced a few transient rises in [Ca2+]i in most cultured cells
and [Ca2+]i oscillation only in one cell. 4. The two components of the slow after-hyperpolarization (AHP) of an action potential
in neurones of freshly isolated ganglia were dependent on extracellular Ca2+ and abolished by Ca2+ channel blockers, Cd2+
or Co2+. 5. The late component of AHP (LAHP), but not the initial component, in 'fresh' neurones increased in area with an
increase in the preceding interval, was abolished by ryanodine (10 microM) and intracellularly injected EGTA, and mimicked
by intracellular injection of Ca2+. 6. A ryanodine-sensitive Ca(2+)-induced Ca2+ release thus exists, operates in response
to an action potential-induced Ca2+ entry and underlies LAHP in rabbit otic ganglion cells. |
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ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.1995.sp020801 |