No abstract

CALCIUM ions are necessary for the transmission of the excitatory state at the neuromuscular junction [Locke, 1894;Overton, 1904;Brown & Harvey, 1939] and at the ganglionic synapse [Bronk, Larrabee, Gaylor & Brink, 1938]. If acetylcholine (ACh.) is the chemical transmitter at these synaptic junctions, a failure of transmission there may be due either to deficient liberation of ACh., or to failure, as a result of altered threshold of the ganglion cell or motor end-plate, of the liberated ACh. to produce its normal effect. The perfused superior cervical ganglion of the cat is a convenient preparation for experiments designed to explore whether either of these possible defects, and if so which of them, is responsible for the failure of transmission which is produced by the withdrawal of calcium. Our experiments show that, when calcium is absent, there is no release of ACh. from the preganglionic nerve endings, either during stimulation of the sympathetic trunk or following the injection of potassium salts. METHODSGanglion perfusion was carried out in the manner previously described [Feldberg & Vartiainen, 1934] with the aid of a small pump of the DaleSchuster type, which provided a pulsatile pressure on the arterial side [MacIntosh, 1938]. The initial perfusion fluid was normal Locke's solution containing eserine sulphate in a concentration of 1: 250,000. When it was desired to expose the ganglion to some modification of Locke's solution, the perfusion system was quickly rinsed and filled with the new solution: this could be done without changing the perfusion pressure or the temperature of the ingoing fluid. More transient effects were obtained by the injection of small volumes of solution into the perfusion fluid 1 Felow of the Rockefeller Foundation.

No abstract

No abstract

THE importance of the actions of quinine on the contractile mechanism of skeletal muscle, and on the processes of neuro-muscular transmission, has been brought into prominence by its effects in certain muscle diseases in human beings [Kennedy & Wolf, 1937;Kolb, Harvey & Whitehill, 1938].That quinine has a pronounced effect upon striated muscle has been recognized for many years. Santesson [1892] found that the sum of work done in response to rhythmical stimulation of the gastrocnemius with single shocks was greater, in both frogs and rabbits, after quinine had been administered, though the height of a tetanus was lowered, and the muscle tired more easily. Secher [1915], by perfusing the hindlimbs of frogs with Locke's (sic) solution containing quinine, found a similar effect upon stimulation with a faradic current of short duration. Fiirth & Schwartz [1909] observed that this increase persisted in the cat after curarization. Brody & Soilman [1923] stated that quinine caused a depression of the response of the isolated frog muscle, as manifested by lowered contraction, more rapid fatigue, and prolongation of the refractory period.In the present paper an account is given of the actions of quinine on the responses to excitation of normal, denervated, and curarized skeletal muscles of the frog, domestic fowl, and cat. METHODSThe mammalian experiments were done on cats decerebrated under preliminary ether, and prepared for arterial injections into the tibialis anterior muscle according to the technique of Brown [1938]. For the study of avian muscle, domestic hens anaesthetized with "pernocton" (10% sol.) were used, the gastrocnemius being arranged for arterial 1 Research Fellow of the American College of Physicians.