Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
Identifieur interne : 002C63 ( Main/Exploration ); précédent : 002C62; suivant : 002C64Relation between intracellular Ca2+ signals and Ca2+-activated Cl− current in Xenopus oocytes
Auteurs : I. Parker [États-Unis] ; Y. Yao [États-Unis]Source :
- Cell Calcium [ 0143-4160 ] ; 1993.
Abstract
Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.
Url:
DOI: 10.1016/0143-4160(94)90067-1
Affiliations:
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<front><div type="abstract" xml:lang="en">Activation of inositol 1,4,5-trisphosphate (InsP3) signalling in Xenopus oocytes causes intracellular Ca2+ mobilization and thereby activates a Ca2+-dependent Cl− membrane conductance. Measurements of cytosolic Ca2+ levels using fluorescent indicators, however, revealed little correspondence with Cl− currents. Intracellular photorelease of InsP3 from a caged precursor evoked transient currents that peaked while the Ca2+-fluorescence signal was rising, and subsequently declined within a few seconds, even though the Ca2+ signal remained elevated much longer. Also, Cl− currents evoked by agonist activation showed transient spikes while a wave of Ca2+ liberation swept across the cell, but then decreased when the Ca2+ signal attained a maximal level. Thus, the Cl− current corresponded better to the rate of rise of intracellular free Ca2+, rather than to its steady state level. Experiments using paired flashes to photolyse caged InsP3 and caged Ca2+ indicated that this relationship did not arise through desensitization or inactivation of the Cl− conductance. Furthermore, fluorescence measurements made at different depths into the cell using a confocal microscope revealed no evidence that a rapid decline of local Ca2+ levels near the plasma membrane was responsible for the decay of Ca2+-activated Cl− current. Instead, Cl− channels may show an adaptive or incremental response to Ca2+, which is likely to be important for the encoding and transmission of information by Ca2+ spikes.</div>
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