Role of Amniotic Fluid Acetylcholinesterase in Screening for Neural Tube Defects

Garry, Ray; Atkins, Jessica; Richardson, Sara; Webb, Brian A.

doi:10.1016/s0140-6736(81)91716-5

Cited by 2 publications

(2 citation statements)

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“…Secretion of AChE from the exposed gastrointestinal tissue could account for its presence in the amniotic fluid in cases of exomphalos (Wald et al, 1980;flale, 1980;Voigtlander et al, 1981;Garry et al, 1981;Crandall et al, 1982;Read et al, 1982). Secretion of BuChE, in addition, would explain why the ratio of BuChE to AChE in amniotic fluid is higher in cases of foetal exomphalos (Goldfine et al, 1983;Wald et al, 1984), compared to cases of foetal neural tube defects where the main change is a greatly increased amount of AChE derived from cerebrospinal fluid .…”

Section: Possible Implicationsmentioning

confidence: 99%

“…Thus several groups who have examined the cholinesterase content of amniotic fluid have detected the presence of AChE (Wald et I'Author for correspondence. al., 1980;Dale, 1980;Voigtlander et al, 1981;Garry et al, 1981;Crandall et al, 1982;Read et al, 1982) in cases of foetal exomphalos. It has been suggested by Wald et al (1980) that the AChE is derived from peripheral nervous tissue such as the intestinal nerve plexi which are exposed to the amniotic fluid in this condition.…”

Section: Introductionmentioning

confidence: 99%

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Secretion of acetylcholinesterase and butyrylcholinesterase from the guinea‐pig isolated ileum

Appleyard

Smith

1989

British J Pharmacology

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Strips of longitudinal muscle from guinea‐pig ileum, retaining Auerbach's plexus, were superfused with oxygenated Krebs solution. Addition of 50 mm KCl led to a pronounced Ca2+‐dependent increase in the activities of both acetylcholinesterase and non‐specific cholinesterase (butyrylcholinesterase) in the perfusate but with no change in lactate dehydrogenase activity. No release of acetylcholinesterase, either spontaneous or K+‐evoked was observed in tissue freed of the nerve plexus, although release of butyrylcholinesterase still occurred. Carbachol induced a marked Ca2+‐dependent increase in the release of acetylcholinesterase but had no effect on the release of butyrylcholinesterase or lactate dehydrogenase. This carbachol‐evoked increase in acetylcholinesterase release was blocked by hexamethonium but not by atropine. Four readily soluble molecular forms of acetylcholinesterase and three soluble molecular forms of butyrylcholinesterase were present in innervated longitudinal muscle strips, but insignificant amounts of acetylcholinesterase were detected in denervated strips of muscle. Only one of the four molecular forms of acetylcholinesterase was recovered in the perfusates. It is concluded that acetylcholinesterase is secreted from the nerves of Auerbach's plexus in response to depolarizing stimuli or to nicotinic cholinergic stimulation, while butyrylcholinesterase is secreted from non‐neural elements, possibly the longitudinal muscle cells, of guinea‐pig ileum in response to a depolarizing stimulus.

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