scholarly journals Intracellular potentials from intrafusal muscle fibres evoked by stimulation of static and dynamic fusimotor axons in the cat

1972 ◽  
Vol 227 (3) ◽  
pp. 709-727 ◽  
Author(s):  
P. Bessou ◽  
B. Pages
1984 ◽  
Vol 346 (1) ◽  
pp. 341-352 ◽  
Author(s):  
L Decorte ◽  
F Emonet-Dénand ◽  
D W Harker ◽  
L Jami ◽  
Y Laporte

It was shown in an earlier paper (7) that if maximal stimulation of either of two different afferent nerves can reflexly excite fractions of a given flexor muscle, there are generally, within the aggregate of neurones which innervate that muscle, motoneurones which can be caused to discharge by either afferent (i. e., motoneurones common to both fractions). The relationship which two such afferents bear to a common motoneurone was shown, by the isometric method of recording contraction, to be such that the activation of one afferent, at a speed sufficient to cause a maximal motor tetanus when trans­mitted to the muscle fibres, caused exclusion of any added mechanical effect when the other afferent was excited concurrently. This default in mechanical effect was called “occlusion.” Occlusion may conceivably be due to total exclusion of the effect of one afferent pathway on the common motoneurone by the activity of the other; but facilitation of the effect of one path by the activation of the other when the stimuli were minimal suggests that, in some circumstances at least, the effect of each could augment and summate with th at of the other at the place of convergence of two afferent pathways. Further investigation, using the action currents of the muscle as indication of the nerve impulses discharged by the motoneurone units, has now given some information regarding the effect of impulses arriving at the locus of convergence by one afferent path when the unit common to both is already discharging in response to impulses arriving by the other afferent path. Our method has been to excite both afferent nerves in overlapping sequence by series of break shocks at a rapid rate and to examine the action currents of the resulting reflex for evidence of the appearance of the rhythm of the second series in the discharge caused by the first when the two series are both reaching the motoneurone.


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.


2003 ◽  
Vol 550 (1) ◽  
pp. 263-278 ◽  
Author(s):  
R. Durbaba ◽  
A. Taylor ◽  
P. H. Ellaway ◽  
S. Rawlinson

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.


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