Effects of catecholamines on early development of the chick embryo: Relationship to effects of calcium and cAMP

Publisher Website
Google Scholar
Abstract
Catecholamines (dopamine or norepinephrine) injected under the blastoderm of the unincubated chick embryo produced a thickened primitive streak and prevented the migration of axial mesoblast after 24 h. The mesoblastic cells that accumulated in the primitive streak contained many intracytoplasmic yolk granules. After 48 h, neural tube, notochord, and somites were severely affected, and their cells appeared loaded with yolk inclusions. Heart, lateral plates, blood cells, and blood vessels differentiated normally. At the onset of gastrulation, the level of glycogen was fivefold lower in catecholamine-treated embryos than in control embryos. Injection of glucose plus dopamine, at equimolar concentrations resulted in normal development both at 24 h and at 48 h. Because adrenegic stimulation of glycogenolysis in differentiated cells is usually mediated by cAMP and/or by calcium, we attempted to determine whether these substances could reproduce the effects of catecholamines. Only calcium was able to produce, to a limited extent, the same morphogenetic disturbances as those produced by catecholamines, whereas the chelating agent, ethylenediamine tetraacetic acid, when administered with dopamine, partially inhibited the effects of catecholamines. An increase in the number of yolk granules was the only common finding among embryos treated with cAMP and catecholamines. Blood and a well differentiated, gastrular endoderm always developed, independently of the nature of the substance with which the embryos had been treated. Morphogenetic disturbances caused by exogenous catecholamines could be due to depletion of glucose. Alternatively, a different metabolic commitment might exist within the diverse populations of cells that constitute the mesoblastic layer.