AbstractThis study was designed to examine the validity of the theory that descent of the tongue, which is presumably induced by fetal muscular movements, is essential for normal closure of the secondary palate in mice. Nulliparous CD1 mice were given the following “muscle‐paralyzing” agents on day 13° of gestation, i.e., 1 day before the onset of the critical period of palate closure: d‐tubocurarine chloride, gallamine triethiodide (Flaxedil), phenobarbital sodium, chlorphenesin carbamate (Maolate), and ethyl ether. The full paralytical effect of each drug was maintained for 42 hours, i.e., until day 15 1/3 of gestation, by means of subsequent fractional doses. Various combinations of barbiturates, anesthetics, and muscle relaxants were also employed. All litters were recovered by laparotomy on day 15° of gestation. The presence of fetuses that were flaccid, limp, apneic, and unresponsive to stimulation was accepted as evidence of transplacental passage of the employed compounds. No cleft palates were found in 656 recovered fetuses. This may be viewed as an indication that muscular activity — either spontaneous or reflexogenic — is not essential for normal closure of the secondary palate in mice.