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  • 1
    Electronic Resource
    Electronic Resource
    The effect of ionophore A 23187 and ruthenium red on tentacle contraction and ultrastructure inDiscophrya collini: Evidence of calcium fluxing from intracellular reservoirs (1983)
    Springer
    Protoplasma 117 (1983), S. 158-166 
    Details
    ISSN: 1615-6102
    Keywords: Calcium ; Contraction ; Discophrya ; Ionophore A 23187 ; Ruthenium red ; Tentacle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The suctorian protozoonDiscophrya collini has contractile tentacles with microfilaments and a central microtubule-lined canal (axoneme). The role of calcium fluxing in tentacle contraction has been investigated using the Ca2+ ionophore A 23187 and ruthenium red (RR), a known inhibitor of certain Ca2+ membrane transport events. Treatment with CaCl2 alone caused tentacle contraction with a threshold at 5 × 10−3 M CaCl2 and a maximum at 5 × 10−2 M CaCl2 with contraction to 32.8% of the original length. In the presence of 5 μM ionophore A 23187 the threshold was lowered to 5 × 10−6 M CaCl2 with a maximum to 19.6% original length at 5 × 10−2 M CaCl2. A 23187 alone induced contraction with a threshold of 3.0 μM and a maximum to 30.5% original length at 10 μM A 23187. Treatment with RR alone had little effect on tentacle length. However, a 10 μM A 23187-induced contraction was partially counteracted by the simultaneous application of RR with a threshold at 2 μM RR and a maximum at 8 μM RR. Removal of the ionophore after induced tentacle contraction resulted in partial re-extension, which was inhibited by RR. Ultrastructural observations indicated that the ionophore and CaCl2-induced contraction processes are indistinguishable. The CaCl2/ionophore treatments led to axonome disruption, interpreted as a consequence of supranormal levels of intracellular Ca2+. X-ray microanalysis of cytoplasmic membrane-bound elongate dense bodies (EDB) showed a high level of Ca2+ in CaCl2-treated cells, little Ca2+ in ionophore-treated cells and intermediate levels in the RR-treated, ionophore/RR-treated and untreated control cells. It is suggested that A 23187 enhances both the uptake of extracellular Ca2+ and the release of Ca2+ from the EDB, the latter being counteracted by RR. These observations support the proposal that the EDB act as Ca2+ reservoirs, and that their Ca2+ fluxing moderates cytosolic Ca2+ levels which mediate a Ca2+-dependent tentacle contraction mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01288354
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Electrically induced tentacle contraction in the suctorian protozoonTrichophrya collini (1989)
    Springer
    Protoplasma 148 (1989), S. 33-40 
    Details
    ISSN: 1615-6102
    Keywords: Contraction ; Electrical stimulation ; Microtubules ; Suctoria ; Trichophrya
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Extracellular electrical stimulation ofTrichophrya collini induces tentacle contraction. There is an inverse relationship between stimulus duration and voltage in producing a threshold response, and at a set voltage the response is graded depending upon duration of stimulus. With a threshold stimulus (6.3 V, 1,000 ms) the response is restricted to the anodal tentacles, and with increasing stimulus intensity or duration the response spreads to the cathodal and finally the intermediate tentacles. With a stimulus of 15 V, 1,000 ms the mean tentacle length is reduced to 28% of the control within 1.2 s. Recordings using intracellular microelectrodes give resting membrane potentials between −10mV and −40mV. Intracellular hyperpolarizing currents of 1nA and 2nA induce tentacle contraction to 50% and 25% of the control length respectively, but depolarizing currents do not induce contraction. SEM studies show that in the initial stages of contraction, only the central region of the tentacle shaft becomes shortened, but on full contraction shortening involves the whole of the shaft. TEM studies show that on contraction no depolymerization of tentacle axoneme microtubules occurs, but that the entire axoneme passes down into the body cytoplasm. These observations are discussed in relation to the possible mechanisms of tentacle contraction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01403989
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  • 3
    Electronic Resource
    Electronic Resource
    Tentacle contraction inDiscophrya collini: The effects of ionophore A23187 and ruthenium red on Ca2+-induced contraction and uptake of extracellular calcium (1984)
    Springer
    Protoplasma 122 (1984), S. 125-131 
    Details
    ISSN: 1615-6102
    Keywords: Calcium ; Contraction ; Discophrya ; Ionophore A23187 ; Ruthenium red ; Tentacles
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary The tentacles of the suctorian protozoonDiscophrya collini are stimulated to contract by externally applied Ca2+. The role of extracellular Ca2+ in tentacle contraction was studied by monitoring45Ca2+ uptake, using ionophore A23187 to facilitate membrane transport of calcium and ruthenium red (RR) as an inhibitor of transport. The degree of tentacle retraction was dependent upon external Ca2+ concentration and studies with45Ca2+ using scintillation counting indicated a linear relationship between external Ca2+ concentration and Ca2+ uptake. Uptake of Ca2+ was enhanced in the presence of the ionophore while RR caused little inhibition.45Ca2+ uptake was only partially inhibited by RR when cells were subjected to a Ca2+, ionophore and RR mixture. Grain counts from light microscope autoradiographs after treatment of cells with45Ca2+/ionophore,45Ca2+/RR or45Ca2+ alone showed heavy, light and intermediate labelling respectively. In all instances the grains were evenly distributed within the cell. These observations are interpreted as supporting the suggestion that the ionophore enhances both the uptake of extracellular Ca2+ and release of Ca2+from an internal source, while the RR could only partially prevent movement of Ca2+ through the plasma mebrane. A model is presented suggesting that tentacle retraction is mediated by cytosolic Ca2+ levels which are determined by the fluxing of Ca2+ across the plasma membrane and the membrane of elongate dense bodies which act as internal Ca2+ reservoirs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01279445
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    Paper (German National Licenses)
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