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Book Chapter

Mechanisms regulating the expression and function of acetylcholine receptor

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons95970

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;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons95089

Sakmann,  Bert
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Witzemann, V., & Sakmann, B. (1988). Mechanisms regulating the expression and function of acetylcholine receptor. In H. Zimmermann (Ed.), Cellular and Molecular Basis of Synaptic Transmission (pp. 453-461). Heidelberg / Berlin: Springer.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-AE47-2
Abstract
Acetylcholine receptors (AChR) are distributed throughout the developing skeletal muscle cell surface, but become highly concentrated at the neuromuscular junction in the innervated adult muscle. Concomitantly, AChRs become metabolically stable and their channel properties change (Edwards 1979; Schuetze and Role 1987). The synthesis of the AChR complex could be regulated on the level of transcription, translation or post-translation, affecting assembly, transport and insertion into the membrane. Regulation at these different levels during development may give rise to the expression of different AChR molecules in embryonic and adult muscle. In addition to AChR-associated changes, epigenetic factors may be involved in regulating or modulating AChR properties. Such factors could reside within the local environment and specific interactions may occur with lipids, proteins or enzymes. AChRs could furthermore communicate with components of the cytoplasmic phase as well as with components and factors originating from the presynaptic nerve terminal. With the introduction of recombinant DNA techniques it became evident that changing levels of the various AChR-subunit specific mRNAs could regulate the expression of different types of AChR (Mishina et al 1986; Evans et al 1987 and references therein).