Contractile responses to direct stimulation of frog slow muscle fibres before and after denervation

1979 ◽  
Vol 382 (1) ◽  
pp. 43-50 ◽  
Author(s):  
N. Lehmann ◽  
H. Schmidt
1986 ◽  
Vol 126 (1) ◽  
pp. 403-422 ◽  
Author(s):  
PETER D. EVANS ◽  
CAMILLA M. MYERS

1. The modulatory actions of FMRFamide and related peptides on tension generated in the extensor-tibiae muscle of the locust hindleg by stimulation of the slow excitatory motor neurone (SETi) depend upon the frequency of stimulation of SETi. They have no effect on the tension induced by the fast motor neurone (FETi) or upon the myogenic rhythm present in this muscle. 2. At low frequencies of SETi stimulation (1Hz and below) the predominant modulatory effects are increases in the amplitude, contraction rates and relaxation rates of twitch tension. At higher frequencies, where twitches summate but tetanus is incomplete (up to 20 Hz) these effects are superimposed upon an increase of maintained tension. 3. FMRFamide increases the amplitude and relaxation rate of slow twitch tension by different amounts in different regions of the extensor muscle. It is likely that the effects of FMRFamide are restricted to slow muscle fibres that are innervated by SETi but not FETi. 4. The modulatory actions of FMRFamide on SETi-induced tension are additive to, but do not potentiate, the modulatory actions of octopamine and proctolin in this muscle. The actions of FMRFamide show some similarities with the modulatory actions of octopamine in this preparation but they are mediated by an independent receptor system that does not change cyclic nucleotide levels. Other actions of FMRFamide are similar to the actions of proctolin.


In the study of the phenomena of anaphylaxis there are certain points on which some measure of agreement seems to have been attained. In the case of anaphylaxis to soluble proteins, with which alone we are directly concerned in this paper, the majority of investigators probably accept the view that the condition is due to the formation of an antibody of the precipitin type. Concerning the method, however, by which the presence of this antibody causes the specific sensitiveness, the means by which its interaction with the antibody produces the anaphylactic shock, there is a wide divergence of conception. Two main currents of speculation can be discerned. One view, historically rather the earlier, and first put forward by Besredka (1) attributes the anaphylactic condition to the location of the antibody in the body cells. There is not complete unanimity among adherents of this view as to the nature of the antibody concerned, or as to the class of cells containing it which are primarily affected in the anaphylactic shock. Besredka (2) himself has apparently not accepted the identification of the anaphylactic antibody with a precipitin, but regards it as belonging to a special class (sensibilisine). He also regards the cells of the central nervous system as those primarily involved in the anaphylactic shock in the guinea-pig. Others, including one of us (3), have found no adequate reason for rejecting the strong evidence in favour of the precipitin nature of the anaphylactic antibody, produced by Doerr and Russ (4), Weil (5), and others, and have accepted and confirmed the description of the rapid anaphylactic death in the guinea-pig as due to a direct stimulation of the plain-muscle fibres surrounding the bronchioles, causing valve-like obstruction of the lumen, and leading to asphyxia, with the characteristic fixed distension of the lungs, as first described by Auer and Lewis (6), and almost simultaneously by Biedl and Kraus (7). But the fundamental conception of anaphylaxis as due to cellular location of an antibody, and of the reaction as due to the union of antigen and antibody taking place in the protoplasm, is common to a number of workers who thus differ on details.


1958 ◽  
Vol 17 (2) ◽  
pp. 134-142 ◽  
Author(s):  
MARY F. LOCKETT ◽  
S. N. GANJU

SUMMARY Pretreatment of salt-maintained adrenalectomized mice for 6 days with 3–6 mg dried thyroid gland, or with 0·25 μg of either l-thyroxine or l-triiodothyronine, per mouse per day, delayed the early onset of both neuromuscular and muscular failure which are characteristic of these animals. Dose-effect curves for the action of thyroxine on the myoneural junctions and striped muscle fibres are given. A concentration of 0·05μg l-triiodothyronine/100 ml. bath fluid antagonized potassium reduction of the maximal twitch of the normal rat diaphragm in response to nerve stimulation, but not in response to direct stimulation of the curarized muscle.


1930 ◽  
Vol s2-73 (291) ◽  
pp. 365-392
Author(s):  
S. B. SETNA

Experimental. 1. The contraction of the adductor-muscle which follows stimulation of the palial nerve is preceded by a marked contraction of the ctenidial axis, so that the gill contracts before the adductor-muscle becomes active. This movement of the ctenidium is abolished if the main branchial nerve is cut near its origin. 2. The gills of Pecten possess a neuromuscular mechanism which is to some extent independent of the rest of the body, so that excised gills when stimulated react in the same way as an attached gill. 3. The lamellae of the gill possess two distinct types of movement. (a) When the surface of the gill is stimulated by contact with a glass rod or by carmine particles, the frontal surfaces of the two lamellae approach each other; the movement very often being executed by the lamella which is not actually being stimulated. The lateral extent of these movements (concertina movements) is roughly proportional to the intensity of the stimulus. Such movements normally appear to transfer the bulk of the material on to the mantle. Separation of the main branchial nerve abolishes these movements. (b) Each principal filament is capable of moving the ordinary filaments to which it is attached. This movement (flapping movement) is due to the movements of the interfilamentar junctions which alternatively move up and down at right angles to their length. This motion is independent of the branchial nerve and can be produced by direct stimulation of very tiny pieces of the individual filaments. 4. The significance of gill movements to feeding habits is discussed. The course of food particles depends on the nature of the stimuli affecting the gill. Histological. 5. The ctenidial axis and the principal filaments have a stratum of anastomosing nerve-cells which appear to form a true nerve-net comparable to that of the mantle. 6. The gill receives nerve-fibres from two sources, the brain and the visceral ganglion. The subsidiary branchial nerve is a structure hitherto unknown in the molluscan gill; so far its function is unknown. Each gill has four main longitudinal nerve-trunks. 7. The osphradium of the gill has a much more extensive distribution than has hitherto been supposed. 8. Two sets of muscles exist at the base of the gill-filaments, and these are responsible for movements of the lamellae. The muscle-fibres are non-striated. 9. The principal filaments are connected to the ordinary filaments by processes containing true muscle-cells, and by these cells movements of the filaments are effected.


1965 ◽  
Vol 209 (5) ◽  
pp. 913-918 ◽  
Author(s):  
Francis J. Klocke ◽  
Gerard A. Kaiser ◽  
John Ross ◽  
Eugene Braunwald

The relative roles of augmented hemodynamic performance and direct stimulation of oxidative metabolism in mediating the increase of myocardial oxygen uptake (MVo2) produced by catecholamines have been examined in an isolated canine heart preparation. The responses of MVo2 to graded doses of isoproterenol, norepinephrine, or epinephrine were determined before and after the induction of cardiac arrest with potassium. Although increases of MVo2 occurred in the arrested state with the larger doses of the amines, they constituted only a small fraction, generally between 5 and 20%, of the increases produced by the same doses of amines when the hearts were beating. It is concluded that while large doses of catecholamines can increase oxidative metabolism of the nonbeating heart by a small amount, the increases of MVo2 produced by catecholamines in the beating heart are due in large part to the hemodynamic alterations which the amines induce.


1985 ◽  
Vol 60 (6) ◽  
pp. 539-547 ◽  
Author(s):  
Willemien Wallinga-De Jonge ◽  
Frans L.H Gielen ◽  
Peter Wirtz ◽  
Paul De Jong ◽  
Jan Broenink

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