The mechanisms of motor end-plate depolarization due to a cholinesterase-inhibiting drug / by W.W. Douglas and W.D.M. Paton.

  • Douglas, W. W.
Date:
[1954?]
Catalogue details

Licence: In copyright

Credit: The mechanisms of motor end-plate depolarization due to a cholinesterase-inhibiting drug / by W.W. Douglas and W.D.M. Paton. Source: Wellcome Collection.

    15/20 (page 339)
    this experiment, the depolarization not only collapsed after the injection of D-tubocurarine, but for a period the end-plate regions became positive with respect to the immediately adjacent regions, the latter still being negative to (C) Fig. 15. Graph of three end-plate depolarizations obtained by stimulating the motor nerve to gracilis (33/sec for 5 sec) after TEPP (500p,g/kg): (a) 1 min after TEPP, before D-tubo¬ curarine; (b) 4 min after TEPP, 1 min after 0-5 mg/kg D-tubocurarine; (c) 9 min after TEPP 2 min after 1*5 mg/kg D-tubocurarine. d 10 mm Fig. 16. The effect of D-tubocurarine on depolarization caused by acetylcholine (500 p,g) in the presence of TEPP (10 mg/kg given 5 min previously). Denervated gracilis, (a) Depolarization caused by acetylcholine and TEPP. Immediately after this D-tubocurarine (5 mg) was injected. (b), (c) and (d) show the effects 116, 328 and 388 sec after D-tubocurarine. The dotted line superimposed on (d) is the effect of injecting a further dose of acetylcholine (500 /ig). the reference electrode (Fig. 16). There was no doubt that these now relatively positive regions corresponded to the end-plate zones since a further dose of acetylcholine elicited a typical depolarization centred on the points previously