Abstract
Acetylcholine (ACh) mediates neurotransmission at the neuromuscular junction and is involved in respiratory control1, notably chemosensitivity2 of central and peripheral origin. The level of ACh at the synaptic cleft and neuromuscular junction is regulated by the enzyme acetylcholinesterase (AChE). Blockade of AChE by organophosphorus compounds produces death by respiratory failure3, but despite the absence of AChE activity in all tissues, AChE (-/-) mice knockout for the gene coding for AChE develop to term4 and survive to adulthood if provided special care5. However, they show many aspects of a cholinergic syndrome, such as pinpoint pupils and muscle tremors5.
Supported by DGA: DSP/STTC 00/34/077.
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© 2004 Kluwer Academic/Plenum Publishers, New York
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Chatonnet, F., Boudinot, E., Chatonnet, A., Champagnat, J., Foutz, A.S. (2004). Breathing Without Acetylcholinesterase. In: Champagnat, J., Denavit-Saubié, M., Fortin, G., Foutz, A.S., Thoby-Brisson, M. (eds) Post-Genomic Perspectives in Modeling and Control of Breathing. Advances in Experimental Medicine and Biology, vol 551. Springer, Boston, MA. https://doi.org/10.1007/0-387-27023-X_25
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DOI: https://doi.org/10.1007/0-387-27023-X_25
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