Search PubMed⌕ Search

Biomedical subjects

E Stefani

Publications and source records attributed to E Stefani.

At least 181 records · Page 10Linked to original sources
PubMed1976

Potassium and calcium conductance in slow muscle fibres of the toad.

Slow muscle fibres in isotonic potassium sulphate saline could be easily repolarized to -90 mV. From this membrane potential a regenerative response could be elicited with short depolarizing pulses. 2. This response is blocked by TEA, suggesting that potassium is the main ion involved. 3. In the presence of TEA, a transient depolarization is recorded when the steady hyperpolarization is withdrawn. This anode break response is dependent upon the external calcium and is blocked by cobalt, suggesting that it is due to a calcium conductance. 4. The membrane conductance change was continuously recorded with short pulses at the end of the hyperpolarization. The membrane conductance decayed with at least two components with an average t1/2 of 1-2 and 6-8 sec. TEA blocked the slow component, and the fast one was dependent upon calcium and was blocked by cobalt.

Animals↗
PubMed1976

Re-innervation of twitch and slow muscle fibres of the frog after crushing the motor nerves.

1. The conduction velocities of individual motor axons innervating twitch and slow muscle fibres of the frog were determined by intracellular recording of junctional potentials elicited by stimulating the motor nerves at two different points. 2. In normal pyriformis muscles twitch and slow fibres were found to be innervated by two distinct populations of motor axons. Twitch fibre axons conducted at 10-18-7 m/sec, while the conduction velocities of slow fibre axons ranged from 0-5 to 5 m/sec (at 7-9 degrees C). The thresholds for electrical stimulation were significantly lower in the fast than in the slow axons population. 3. Following denervation by crushing the sciatic nerve fast axons which re-innervated the muscle had lower conduction velocities than normal but could still be identified. These lower conduction velocities were measured proximal to the site of the crush and did not recover over a period of 446 days. 4. Fast motor axons regenerated more quickly than slow axons and re-innervated twitch as well as slow muscle fibres non-selectively. About 1 month later slow axons re-established synaptic contacts with slow (and some twitch) muscle fibres. Simultaneous re-innervation by fast and slow motor axons was occasionally observed in slow muscle fibres. Finally, the slow muscle fibres were innervated by slow axons only, while synapses of fast axons could no longer be found in this type of muscle fibre. 5. Action potentials were observed in denervated as well as in re-innervated slow muscle fibres; they disappeared as re-innervation progressed. 6. It is concluded that non-selective re-innervation of slow muscle fibres is present in the frog; it is, however, a transient phenomenon followed by restoration of the original innervation pattern.

Action Potentials↗
PubMed1974

Twitch potentiation by potassium contractures in single muscle fibres of the frog.

1. The modifications of isometric twitches after K contractures have been studied in single muscle fibres from frog muscles.2. The twitch was greatly enhanced and somewhat prolonged after a conditioning K contracture. This potentiating effect was more evident in fibres having low values of the ratio control twitch tension/tetanus tension (P/P(0)).3. In most of the fibres, the time course of the decay of the potentiation phenomenon could be represented by the sum of three negative exponentials with average half-times of 9.1, 40 and 485 sec.4. Between 3 and 10 min after the onset of the twitch potentiation the resting potential and action potential were unchanged.5. Mn blocked the K contractures and prevented the onset of the twitch potentiation.6. 40-140 sec after inducing a K contracture with 30 or 40 mM-K, a second exposure to the same [K] evoked a tension equivalent only to 57% of the first one. This partial refractoriness of the fibres is not seen when both contractures were elicited with 190 mM-K, and contrasts with the full recovery and potentiation of the twitch after a K contracture.

Action Potentials↗
PubMed1973

Effects of manganese on the electrical and mechanical properties of frog skeletal muscle fibres.

1. The effects of Mn on the electrical and mechanical properties of frog muscle fibres have been studied.2. In normal saline 10 or 20 mM-Mn hyperpolarized the fibres and had no effect on the membrane resistance. In isotonic K(2)SO(4) saline, Mn increased the membrane resistance indicating that this agent reduced the conductance to K.3. The action potential is prolonged by Mn while the overshoot amplitude is unaffected. The threshold of the action potential is shifted to more positive values of membrane potential.4. The isometric twitch is reduced by 45% in 10 mM-Mn; this effect is observed within 8 sec of the application.5. Mn (10 mM) reduced K contractures induced by 40 or 75 mM-K (constant [K].[Cl] product) and shifted to the right in a parallel manner the curve tension vs. log K concentration. The calculated mechanical threshold for K contractures was shifted from -48 to -33 mV.6. Caffeine contractures (3-4 mM) and supramaximal K contractures (190 mM-K) were unaffected by 10 mM indicating that contractile proteins and the ability of the sarcoplasmic reticulum to release Ca are not impaired.7. It is concluded that Mn is mainly affecting the excitation-contraction coupling by altering the mechanical threshold. Since Mn reduces the permeability to Ca in several excitable membranes, it is suggested that the mechanical threshold depends on the entry of Ca to the muscle.

Action Potentials↗
PubMed1971

Electrophysiological studies of neuromuscular transmission in hereditary 'motor end-plate disease' of the mouse.

1. Studies have been made on isolated nerve-muscle preparations from mice with hereditary ;motor end-plate disease'.2. Spontaneous fibrillation was observed in the isolated preparation.3. Muscles gave only a weak twitch or failed to contract in response to nerve stimulation. Direct stimulation of muscles caused a twitch response which had a slower time course than normal. Peripheral nerve conduction was normal.4. Intracellular recording from single muscle fibres showed that with longer survival of the animal an increasing proportion of fibres failed to show end-plate potentials or action potentials in response to nerve stimulation.5. Miniature end-plate potentials (m.e.p.p.s) were recorded in almost all muscle fibres including those in which neuromuscular transmission had failed. The frequency of m.e.p.p.s was greater than normal, was not increased by tetanic stimulation of the nerve but was increased by a raised external potassium concentration.6. Muscle fibres were supersensitive to acetylcholine.7. The results suggest that the muscular weakness in this disease is due to the failure of nerve action potentials to invade motor nerve terminals so that muscle fibres become ;functionally denervated'.

Acetylcholine↗
PubMed1971

Induction of the action potential mechanism in slow muscle fibres of the frog.

1. The electrical and structural characteristics of ;slow' muscle fibres of the frog were studied in normal and denervated muscles, and in muscles undergoing re-innervation by a mixed nerve containing large and small motor axons.2. In agreement with previous studies, slow fibres in normally innervated muscles were incapable of producing action potentials.3. Approximately 2 weeks after the sciatic nerve was transected or crushed, slow muscle fibres acquired the ability to generate action potentials. These fibres were positively identified as belonging to the slow type, because their passive-electrical and ultrastructural characteristics remained essentially unchanged after the operations.4. The action potential mechanism induced in slow fibres is sodium-dependent, and is blocked by tetrodotoxin.5. After long-term re-innervation by a mixed nerve, slow fibres lose their acquired ability to generate action potentials, presumably because small motor axons re-establish connexion with the fibres.6. It is concluded that the action potential mechanism of slow muscle fibres is under neural control, and is normally suppressed by small motor axons.

Action Potentials↗