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M Siebler

Publications and source records attributed to M Siebler.

77 records · Page 5Linked to original sources
PubMed1988

The effect of D600 on potassium contractures of slow muscle fibres of Rana temporaria.

(1) The effect of 30 microM D600 on the amplitude and time course of isometric contractures was studied in single slow fibres of Rana temporaria. (2) D600 only slightly reduced the amplitude of contractures evoked with 30 or 95 mM K-Ringer's. Maintenance of tension was strongly impaired by D600 only during exposure to 95 mM K. The caffeine contracture was not affected. (3) Addition of 10 mM Ca2+ or other divalent cations to the medium strongly counteracted the effect of D600 on maintained tension. The order of efficiency was Ca2+ = Ni2+ greater than Co2+ greater than Mn2+ much greater than Mg2+. (4) During 2 min exposure to 95 mM K-Ringer's the slow fibres inactivated to a variable degree; recovery from inactivation in normal Ringer's proceeded with a half time of the order of 1 min, while in the presence of D600 recovery was prolonged 3.3 to 27 times. (5) It is concluded that the effect of D600 on the contractile behaviour of slow fibres from Rana temporaria is predominantly due to a prolongation of the inactivated state. It is suggested that D600 binds to a site at the outer membrane surface which also binds divalent cations and determines the degree of contractile inactivation during exposure to potassium. Blocking of Ca2+ channels is unlikely to be the mechanism of this D600-effect.

Animals↗
PubMed1987

D600 prolongs inactivation of the contractile system in frog twitch fibres.

(1) Single twitch fibres were dissected from tibialis muscles of Rana temporaria and used to study the effect of D600 (gallopamil) on potassium-induced contractures. (2) 95 mM K-Ringer's was applied for 8-15 s at intervals of generally 2.5-5 min; at temperatures of 6-8 degrees C and in the absence of D600 the amplitude of the contractures remained fairly constant. After pretreatment with D600 (30 microM) a single (conditioning) K-contracture was sufficient to 'paralyze' the fibres (cf. Eisenberg et al. 1983). (3) Complete paralysis could also be achieved at 18-20 degrees C. In three fibres a single conditioning K-application was sufficient; in two more fibres two or three conditioning K-applications were required. (4) D600-paralysis could not only be achieved with high K-concentrations but also by conditioning with sub- or suprathreshold K-concentrations (20-40 mM); the duration of the conditioning periods required to induce complete paralysis was approximately the same before and after D600-treatment. (5) Contractures were partially abolished by application of 20-40 mM K-Ringer's for short conditioning periods; after D600-treatment the degree of contracture loss was similar. (6) At low temperature the state of partial or complete paralysis induced by subthreshold K-concentrations and D600 was maintained for long periods of time. (7) The presence of 10 mM Ca2+ did not protect the fibres from being paralyzed by treatment with D600 and high K-Ringer's at low temperature; however, more than one conditioning K-application was required.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1986

Induction of the action potential in innervated slow muscle fibers of the frog. Effects of tetrodotoxin, vincristine and colchicine.

Experiments were made to induce action potentials in innervated slow muscle fibers of Rana temporaria. Drugs were applied to the sciatic nerve or its spinal roots by one of the following methods: implantation of a silastic cuff containing tetrodotoxin (TTX); subepineural injection of TTX combined with subcutaneous injections of vincristine; and epineural application of colchicine or vincristine. Twelve to 50 days later slow fibers responded to direct or indirect stimulation with an action potential. A substantial number of these fibers were innervated by 2 or 3 slow motor axons. It is concluded that these effects of TTX and colchicine (vincristine) are due to inhibition of the axoplasmic transport of an unidentified substance. The results support the hypothesis that the inexcitability of normal slow fibers is due to a 'trophic' effect of their motor axons.

Action Potentials↗