OLSON, W.M.*; HALL, B.K.: Heart morphogenesis and neural crest cell migration in cardia bifida chick embryos.
During normal development, cardiac neural crest cells migrate from their position over the neural tube, through the pharyngeal region and into the heart, where they contribute to the septation of the heart and outflow tract, as well as to the cardiac valves and great vessels. The primitive heart tube of higher vertebrates is the result of migration and fusion of bilateral cardiac primordia along the ventral midline of the embryo. Cardia bifida, or “split hearts” can be induced by cutting the anterior intestinal portal (AIP) early in development, thus preventing fusion of the heart primordia. Bifid embryos posses two lateral hearts instead of one median, and pharyngeal development is disrupted. In vitro methods, in which embryos were cultured ventral side up on thin albumin, produced cardia bifida (100%), but did not allow development past ST 11. Culturing the embryos on semisolid medium (1:1 agar:albumin) permitted development to ST 16. In ovo techniques, in which the AIP was cut either from the lateral dorsal side of the embryo or by cutting straight through the dorsal midline, proved less successful at producing bifida (up to 50%), but prolonged survival until ST 24. No completely bifid embryos survived past ST 17. HNK-1, a neural crest marker, was used to analyze whether migration of the cardiac crest is altered in cardia bifida embryos. Initial results suggest that the distribution of HNK-1 positive cells is similar in experimental, sham, and undisturbed embryos, with the following exceptions. Starting at stage 16, experimental embryos show transverse streams of positive cells crossing the dorsal hindbrain; in ST 16-20, HNK-1 is limited to the proximal regions of the pharyngeal arches and does not extend as far distally as in the non-experimental groups.