Changes in holding and ion‐channel currents during activation of an ascidian egg under voltage clamp

Kozuka, Masao; Takahashi, Kunitaro

doi:10.1113/jphysiol.1982.sp014072

Cited by 30 publications

(19 citation statements)

References 26 publications

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“…In Boltenia eggs, L-type-like current persists until the 8-cell stage, whereas Nav currents disappear by the 8-cell stage [55]. In Halocynthia, however, the second type (T-type-like current) quickly disappears just after fertilization, whereas the first type (Ca current through Nav channel) rapidly increases after fertilization [56]. In Ciona intestinalis, L-type like current, partially DHP-sensitive, disappears before the two cell stage, whereas the fast-inactivating Ca current persists until later.…”

Section: Cav Channel From Eggs Early Embryos and Non-muscle-lineage mentioning

confidence: 99%

The Ascidian Dihydropyridine-Resistant Calcium Channel as the Prototype of Chordate L-Type Calcium Channel

et al. 2003

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This review describes recent findings on voltage-gated Ca channel (Cav channel) cloned from ascidians, the most primitive chordates. Ascidian L-type like Cav channel has several unusual features: (1) it is closely related to the prototype of chordate L-type Cav channels by sequence alignment; (2) it is resistant to dihydropyridine due to single amino acid change in the pore region, and (3) maternally provided RNA putatively encodes a truncated protein which has remarkable suppressive effect on Cav channel expression during development. Ascidian Cav channel will provide a useful molecular clue in the future to understand Ca²⁺-regulated cell differentiation and physiology with the background of recently defined ascidian genome and molecular biological tools.

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Section: Cav Channel From Eggs Early Embryos and Non-muscle-lineage mentioning

confidence: 99%

The Ascidian Dihydropyridine-Resistant Calcium Channel as the Prototype of Chordate L-Type Calcium Channel

et al. 2003

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“…Previously, ion channels in unfertilized eggs (Okamoto, Takahashi & Yoshii, 1976) and their changes after fertilization (Kozuka & Takahashi, 1982) have been described in the ascidian, using the two-electrode voltage-clamp technique and, more recently, the whole-cell patch-clamp technique (Block & Moody, 1987). Membrane properties of ascidian gastrulae have also been studied by intracellular recording from cells in whole embryos in which all the blastomeres are tightly electrically coupled, and the existence of inward-rectifier K+ channels at the gastrula stage has been suggested (Miyazaki, Takahashi, Tsuda & Yoshii, 1974).…”

Section: Invard-rectifier K+ Channel In Embryogenesis 247mentioning

confidence: 99%

Neural induction suppresses early expression of the inward‐rectifier K+ channel in the ascidian blastomere.

Okamura

Takahashi

1993

The Journal of Physiology

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SUMMARY1. Early expression of ion channels following neural induction was examined in isolated, cleavage-arrested blastomeres from the ascidian embryo using a twoelectrode voltage clamp. Currents were recorded from the isolated, cleavage-arrested blastomere, a4-2, after treatment with serine protease, subtilisin, which induces neural differentiation as consistently as cell contact.2. The inward-rectifier K+ current increased at the late gastrula stage shortly after the sensitive period for neural induction both in the induced (protease-treated) and uninduced cells. Ca2+ channels, characteristic of epidermal-type differentiation, and delayed-rectifier K+ channels and differentiated-type Na+ channels, characteristic of neural-type differentiation appeared much later than the inward-rectifier K+ channels, at a time corresponding to the tail bud stage of the intact embryo.3. When cells were treated with subtilisin during the critical period for neural induction, the increase in the inward-rectifier K+ current from the late gastrula stage to the neurula stage was about three times smaller (3-67 + 1-74 nA, mean + S.D., n = 14) than in untreated cells (1P25+ 3 10 nA, n = 26). The same changes in the inward-rectifier K+ channel were also observed in a4-2 blastomeres which were induced by cell contact with an A4-1 blastomere. However, when cells were treated with subtilisin after the critical period for neural induction, the amplitude of the inward-rectifier K+ current was the same as in untreated cells. Thus the expressed level of the inward-rectifier K+ channel was linked to the determination of neural or epidermal cell types.4. There was no significant difference in the input capacitance of induced and uninduced cells, indicating that the difference in the amplitude of the inward-rectifier K+ currents derived from a difference in the channel density rather than a difference in cell surface area.5. The expression of the inward-rectifier K+ channel at the late gastrula stage was sensitive to oc-amanitin, a highly specific transcription inhibitor. In both induced and uninduced cells, injection of a-amanitin at the 32-cell stage reduced the current density of the inward-rectifier K+ channel to about 2 nA/nF, corresponding to 13 % of that recorded from uninjected cells. By contrast, the expression of the fast-* To whom reprint requests should be sent. MS 99839 PHY 463 Y. OKAMURA AND K. TAKAHASHI inactivating-type Na' current. which transiently increased along with the inwardrectifier K+ channel, was resistant to a-amanitin injection. 6. The dose of x-amanitin injected was controlled by monitoring co-injected fluorescent dye, fura-2. The dose of x-amanitin required for 50% suppression of the inward-rectifier K+ current was 3-0 ng/ml. This was close to that reported for in vitro inhibition of RNA polymerase-JI from eukaryotic cells, if the difference in temperature was taken into account.7. In the uninduced cells, injection of x-amanitin later than the 32-cell stage partially suppressed the expression of the inward-rectifier...

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“…If transferred into sea water maintained at 10 'C, the animals spawned eggs and sperm at about noon on the following day. Eggs were fertilized by mixing with sperm from another animal and the resulting embryos were cultured in sea water at 8 'C on a slowly moving table (0 3 Hz) as described previously (Takahashi & Yoshii, 1981;Kozuka & Takahashi, 1982;. The nomenclature and morphological features of ascidian embryos at various stages of development at 9 'C have been described previously (Ohmori & Sasaki, 1977).…”

Section: Embryosmentioning

confidence: 99%

Development of ionic channels and cell‐surface antigens in the cleavage‐arrested one‐cell embryo of an ascidian.

Hirano

Takahashi

1987

The Journal of Physiology

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SUMMARY1. The developmental time course of the appearance of ionic channels was studied with the voltage-clamp technique at 8°C in ascidian embryos in which cleavage was arrested with cytochalasin B immediately after fertilization. The ontogeny of cell-surface antigens was also studied using monoclonal antibodies in both normal and cleavage-arrested embryos. The cleavage-arrested 1-cell embryo differentiates into a cell of epidermal type expressing Ca2+, anomalous rectifier and Ca2+-induced K+ channels, and cell-surface antigens against tunic.2. The size of the Sr2+ current through egg-type Ca2+ channels decreased during the initial 15 h and disappeared. At about 45 h a Sr2+ current reappeared; the properties of these new channels were different from those of the egg type and were considered to be those of differentiated epidermal Ca2+ channels.3. Na+ currents also decreased during the first 15 h, and then tended to increase, reaching a peak at about 35 h before decreasing again and finally disappearing.4. The K+ current through anomalous rectifier channels gradually increased in amplitude, reached a peak at about 35 h and then slightly decreased to a minimum at 45 h. It then increased with further development.5. The K+ current through the Ca+-induced K+ channels appeared at 50 h and then increased.6. Input capacity started to increase at 15 h, attained a peak value of three times that of the egg at about 35 h, and then decreased.7. Two anti-tunic monoclonal antibodies, Cl and 2C5, were obtained. Cl bound only to the tunic; 2C5 bound to the tunic and to the cytoplasm of epidermal cells.8. C I antigens first appeared on the surface of the epidermis of the normal embryos and on the surface of the cleavage-arrested 1-cell embryo at about 45 h, and then increased in amount.9. In the normal embryo 2C5 antigen was first detected at about 40 h inside epidermal cells. It started to accumulate on the epidermal surface at about 45 h and then appeared also in the tunic. In the cleavage-arrested embryo the antigen was first detected at about 50 h, and became more intensely stained as development proceeded.10. Actinomycin D, an RNA synthesis inhibitor, inhibited only those changes in 1T. HIRANO AND K. TAKAHASHI later developmental phase, such as the appearance of the differentiated Ca2+ channels, the increase of anomalous rectifier channels after 45 h, the appearance of Ca2+-induced K+ current and of both tunic antigens, when applied before 25 h. Later application allowed the development of these currents and antigens to some extent. 11. The results indicate that the critical developmental changes in ionic channels occur synchronously and that development can be divided into actinomycin-D-insensitive earlier phases and an actinomycin-D-sensitive later phase. They also suggest that transcription of mRNAs for both tunic antigens and ionic channels started simultaneously, as did the secretion of tunic antigens and the incorporation of cell-type-specific ionic channels into plasma membrane.

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Changes in holding and ion‐channel currents during activation of an ascidian egg under voltage clamp

Cited by 30 publications

References 26 publications

The Ascidian Dihydropyridine-Resistant Calcium Channel as the Prototype of Chordate L-Type Calcium Channel

The Ascidian Dihydropyridine-Resistant Calcium Channel as the Prototype of Chordate L-Type Calcium Channel

Neural induction suppresses early expression of the inward‐rectifier K+ channel in the ascidian blastomere.

Development of ionic channels and cell‐surface antigens in the cleavage‐arrested one‐cell embryo of an ascidian.

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