Search

Amphibian sympathetic ganglion cells produce hyperpolarizing and depolarizing responses to adrenaline. Two kinds of adrenergic receptors responsible for the production of these responses appear to occur at different sites on the cell surface. The hyperpolarizing response is produced by changes in the sodium pump, presumably an electrogenic sodium pump, whereas the depolarizing response is produced by changes in the membrane permeability to certain ions.

In mice the spontaneous motor activity tested by the photo-cell counter method was depressed by a chronic administration of lithium and was accelerated by a chronic administration of rubidium or cesium. These effects of lithium and rubidium are in accord with the therapeutic effects of these alkali metals on manic and depressive psychoses, respectively. Cesium, like rubidium, may be worth for clinical evaluation as an antidepressant agent in man.

Cardiotonic effect of proscillaridin A, cardiac glycoside derived from a squill, was tested in some methods. 1. Lethal doses (Hatcher doses) of proscillaridin A were 0.142mg/kg in cats, 0.152mg/kg in dogs, and 0.484mg/kg in rabbits, whereas the dose of g-strophanthin was 0.104mg/kg in cats. 2. 3.16×10-8 Molar concentration of proscillaridin A showed a persistent 60% increase of contractile force in cat papillary muscle preparation. 3. Contractile force of left ventricular muscle showed 9% increase after the second administration (total proscillaridin A 0.04mg/kg) in phenobarbital induced myocardial depression. 4. The ratio between the maximum rate of development isometric tension (dp/dt) and a constant fraction of the integrated isometric tension developed (IIT) showed 12% increase after the second administration of proscillaridin A.

In amphibian sympathetic ganglia, a transient membrane depolarization was produced at the intraganglionic portion of preganglionic nerve fibers when ganglion cells were activated antidromically. Such a depolarization was produced by the action of a chemical transmitter which was not acetylcholine but an unidentified substance released from some cellular elements in the ganglion. These results suggested that the preganglionic nerve terminals possess some noncholinergic receptors in addition to the cholinergic presynaptic receptors.

A tetanic antidromic stimulation of a group of ganglion cells in a nicotinized bullfrog sympathetic ganglion induced a slow and small hyperpolarization in the unstimulated, adjacent group of ganglion cells. Except for its enhancement by atropine, the hyperpolarization had a property essentially similar to that of the slow IPSP. In addition, the afterdischarge of the adjacent ganglion cells, which was elicited by preganglionic stimulation, in the presence of nicotine and atropine was suppressed at the time the hyperpolarization was generated in these neurons. The results indicate that the antidromic postganglionic volleys cause the liberation of a noncholinergic transmitter substance from the activated ganglion cells or possibly from some interneurons, and that the transmitter brings about in the unstimulated, neighboring ganglion cells a slow hyperpolarization which inhibits the generation of the after-discharge. Thus it is evident that a functional interrelation exists among the ganglion cells in a sympathetic ganglion.