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Breathing without acetylcholinesterase

Authors :: Arnaud Chatonnet
Fabrice Chatonnet
Jean Champagnat
Eliane Boudinot
Arthur S. Foutz
Différenciation Cellulaire et Croissance (DCC)
Institut National de la Recherche Agronomique (INRA)-Université Montpellier 2 - Sciences et Techniques (UM2)
J. Champagnat (Editeur)
M. Denavit-Saubié (Editeur)
G. Fortin (Editeur)
A.S. Foutz (Editeur)
M. Thoby-Bisson (Editeur)
Neurobiologie génétique et intégrative (NGI)
Centre National de la Recherche Scientifique (CNRS)
Institut de Neurobiologie Alfred Fessard (INAF)
Département de Physiologie Animale (PA)
Institut National de la Recherche Agronomique (INRA)
Département de Physiologie Animale (INRA)
PERIGNON, Alain
Source :: Post-genomic perspectives in modeling and control of breathing, Post-genomic perspectives in modeling and control of breathing, 551, Kluwer Academic Publisher, 2004, Advances in Experimental Medicine and Biology, Advances in Experimental Medicine and Biology, Advances in Experimental Medicine and Biology, Kluwer, 2004, 551, pp.165, Advances in Experimental Medicine and Biology ISBN: 9780306485077
Publication Year :: 2004
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.