Distribution pattern of acetylcholinesterase in early embryonic chicken hearts

Abstract

To study the developmental appearance of acetylcholinesterase in early embryonic hearts, an enzyme-histochemical study was carried out in chicken embryos ranging from cardiogenic plate to late tubular stages. Initially acetylcholinesterase is present in all cells of the (future) myocardium. When 13-14 pairs of somites have developed, i.e., shortly before blood propulsion starts, acetylcholinesterase selectively disappears from the ventral and lateral wall of the developing ventricle. Slightly later, when 18-19 pairs of somites have developed, acetylcholinesterase also disappears from the dorsal and anterior wall of the atrium. High concentrations of acetylcholinesterase remain present in the outflow tract and lower concentrations in a continuous tract along the lesser curvature of the heart, the atrial side of the atrioventricular canal, and the left wall of the atrium. In late tubular stages of heart development, acetylcholinesterase is reexpressed in the inner myocardial layer of the ventricle, i.e., in the developing trabeculae and the ventricular side of the atrioventricular canal, where it is continuous with the acetylcholinesterase-expressing cells of the atrial side of the atrioventricular canal. The expression pattern of acetylcholinesterase in early embryonic chick hearts coincides with that of areas that control the conduction of the impulse and may reveal a cholinergic signal transduction system that is responsible for a coordinated contraction pattern of the myocardium prior to the development of the definitive conductive system.

Origin and development of the atrioventricular myocardial lineage: Insight into the development of accessory pathways

“…The different cell population in the heart could be distinguished on the basis of their ultra-structure using electron microscopy (Virágh and Challice, 1977a;Virágh and Challice, 1977b;Virágh and Challice, 1980;Virágh and Challice, 1982), glycogen content (Virágh and Challice, 1980), and difference in enzyme activity (Thornell et al, 1984;Lamers et al, 1987;Lamers et al, 1990). Using these differences, the atrioventricular canal region could be identified in consecutive stages of development and its changing aspects monitored.…”

Distribution of acetylcholinesterase activity in the rat embryonic heart with reference to HNK-1 immunoreactivity in the conduction tissue

“…However, there is some evidence that AChE activity exists in the embryonic and neonatal heart before innervation (Navaratnam 1965;Gyevai 1969;Finlay and Anderson 1974;Drews 1975;Lamers et al 1987Lamers et al , 1990. Further, many authors have hypothesized that the transient embryonic AChE activity might be involved in morphogenesis in the embryo (Drews 1975;Vanittanakom and Drews 1985;Kaehn et al 1988;Oettling etal.…”

Distribution of antigen epitopes shared by nerves and the myocardium of the embryonic chick heart using different neuronal markers

“…We were also interested in the neuronal elements as well as nonneuronal tissues in the embryonic myocardium that are stained with the antibodies used here. In literature, markers have been described to stain both cardiac nerve tissue and areas of the myocardium developing into the conduction system such as NF-M (Gorza et al, 1988;Vitadello et al, 1996), AchE (Lamers et al, 1987(Lamers et al, , 1990, PSA-NCAM (Watanabe et al, 1992;, EAP-300 (McCabe et al, 1995), and the markers showing nearly identical expression in the human atrioventricular conduction system GLN-2 (Wessels et al, 1992) and HNK-1 (Gorza et al, 1988;Ikeda, 1990;Luider et al, 1993;Blom et al, 1999). Because of the expression of these neurogenic and crestassociated markers in conduction tissue, some authors proposed a neuroectodermal origin of conduction cells (Gorza et al, 1988;Filogamo et al, 1990).…”