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The transfer of "Sr from mother to offspring througFn the placenta during intra-uterine life arnd through mothers milk during nursing was observed in experimentalmice.Three groups of female mice were injected intraperitoneally with 2, uni of "Sr ixr0-5 ml salune solution as a single tracer dose atnd mated at differ"ent intervals after injection.The amounts of"Sr accumulated in the youmng at birth were 0.087, 0.067, and 0.047per cent or the ctose in those derived trorn mice mated t -2 weeks, 2 -3 weeks, ana 4-5weeks after "Sr unjectiort, respectively. From these results, it was apparent that tlaeshorter the interval betvveen injection and parturition, the greater became the "Sr con-tent in the young at birth.In the young brought forth by an "Sr-contamiuaa-ted mother and nursed with herbreast rnulk, the accumulation of "Sr increased rapidly on the 3rd day after birth. The"St retained by the suckling was derived partially frorn placental transfer and partially1f0rT1 mothers milk. Thorn relative contributions by the transplacental and milk-borne"81 taken by the suckling during the nursing period were calculated. The contributionof transplacental "Sr decreased rapidly after birth. On the contrary, that of milk-borne"Sr increased during nursing.

In the preceding articles (1-4), a dual mode of paralyzing action of candicine (maltoxin) on the frog muscles was reported, i.e., an overall depolarization of the muscle fiber membrane and a depression of sensitivity of the endplate membrane to acetylcholine. On the other hand, candicine has been known as a nicotine-like drug without any detail analysis (5-17). Present experiments have been carried out to elucidate the mode of the ganglion stimulating action of candicine in comparison with some other ganglionic stimulants.

Maltoxin, an amine obtained from brew malt rootlet, has been reported to have a strong contrac ile effect on the frog rec us muscle (1). Crystalline powder of maltoxin hydrochloride was isolated from the crude component, and was found to produce a peripheral paralysis in the frog. This peripheral action of maltoxin was revealed to be an effect on the neuromuscular junction. In the present paper the effect of maltoxin on the nerve-sartorius and the rec us muscle preparations of the frog is described.

Maltoxin, an amine obtained from brew malt rootlet, causes a neuromuscular block in the frog. Its mode of action on the frog's sartorius muscle has been studied mainly with the aid of intracellular microelectrodes. Maltoxin of 10–5 concentration caused an over-all depolarization of the muscle fibers; therefore, direct and indirect stimulations of the muscle were ineffective in producing muscle action potential. Progressive repolarization took place thereafter and the muscle became excitable by direct stimulation, though indirect stimulation remained ineffective for a long period of time. Small end-plate potentials observed could not be explained in terms of depolarization. It was found that the sensitivity of the end-plate membrane to acetylcholine was effectively depressed by maltoxin, and that this is responsible for the persistent neuromuscular block. The initial over-all depolarization caused by maltoxin was fairly antagonized by a previous treatment with d-tubocurarine. It is concluded that maltoxin has a dual mode of action, having some resemblance to acetylcholine, decamethonium, succinylcholine and nicotine.