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Changes in acetylcholinesterase molecular forms during the embryonic development of Torpedo marmorata

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Witzemann,  Veit
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society;
Molecular anatomy of the neuromuscular junction, Max Planck Institute for Medical Research, Max Planck Society;
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Witzemann, V., & Boustead, C. (1982). Changes in acetylcholinesterase molecular forms during the embryonic development of Torpedo marmorata. Journal of Neurochemistry, 39(3), 747-755. doi:10.1111/j.1471-4159.1982.tb07956.x.


Cite as: https://hdl.handle.net/21.11116/0000-0000-E966-7
Abstract
Multiple molecular forms of acetylcholinesterase from electric organ and electric lobe of Torpedo marmorata were examined at various developmental stages by sucrose density sedimentation. Four major forms were characterized by their apparent sedimentation coefficients of 6 S, 11 S, 13 S, and 17 S. Embryonic lobe possessed at early stages predominantly the 11 S form. With maturation the 17 S form became the most abundant. The early embryonic stages of the electric organ were characterized by predominating amounts of 6 S and 11 S forms. With differentiation of the postsynaptic membrane of the developing electrocytes, 13 S and 17 S forms replaced the slower-sedimenting forms. Concomitant with the formation of synaptic contacts, a transient increase in the 13 S form was followed by a dramatic accumulation of rapid-sedimenting 17 S form. The establishment of fully functional synapses was accompanied by an increase in the amount of the hydrophobic 6 S form. At birth, equal amounts of 6 S and 17 S form were found, with the other forms present in only trace amounts. The observed characteristic changes correlated with morphological and physiological events, indicating a close functional relationship between the accumulation of the 17 S form and synapse formation and the accumulation of the 6 S form and onset of function.