{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T06:40:20Z","timestamp":1790059220127,"version":"4.0.1"},"reference-count":63,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,8,3]],"date-time":"2012-08-03T00:00:00Z","timestamp":1343952000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2012,9]]},"abstract":"<jats:sec><jats:label\/><jats:p><jats:italic>J. Neurochem<\/jats:italic>. (2012) <jats:bold>122<\/jats:bold>, 1065\u20131080.<\/jats:p><\/jats:sec><jats:sec><jats:title>Abstract<\/jats:title><jats:p>Acetylcholinesterase (AChE) rapidly hydrolyzes acetylcholine. At the neuromuscular junction, AChE is mainly anchored in the extracellular matrix by the collagen Q, whereas in the brain, AChE is tethered by the proline\u2010rich membrane anchor (PRiMA). The AChE\u2010deficient mice, in which AChE has been deleted from all tissues, have severe handicaps. Surprisingly, PRiMA KO mice in which AChE is mostly eliminated from the brain show very few deficits. We now report that most of the changes observed in the brain of AChE\u2010deficient mice, and in particular the high levels of ambient extracellular acetylcholine and the massive decrease of muscarinic receptors, are also observed in the brain of PRiMA KO. However, the two groups of mutants differ in their responses to AChE inhibitors. Since PRiMA\u2010KO mice and AChE\u2010deficient mice have similar low AChE concentrations in the brain but differ in the AChE content of the peripheral nervous system, these results suggest that peripheral nervous system AChE is a major target of AChE inhibitors, and that its absence in AChE\u2010 deficient mice is the main cause of the slow development and vulnerability of these mice. At the level of the brain, the adaptation to the absence of AChE is nearly complete.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1471-4159.2012.07856.x","type":"journal-article","created":{"date-parts":[[2012,7,2]],"date-time":"2012-07-02T20:54:02Z","timestamp":1341262442000},"page":"1065-1080","source":"Crossref","is-referenced-by-count":38,"title":["Near\u2010complete adaptation of the PRiMA knockout to the lack of central acetylcholinesterase"],"prefix":"10.1111","volume":"122","author":[{"given":"Vladimir","family":"Farar","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Franziska","family":"Mohr","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie","family":"Legrand","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Boris","family":"Lamotte 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