Worm Breeder's Gazette 12(1): 47 (September 1, 1991)
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
We examined the genetic regulation of the flow of acetylcholine in the C. elegans nervous system. Several genes ( unc-17 , unc-18 , unc-41 , unc-11 , unc-13 , unc-63 , unc-64 ) may contribute to the function because these mutations accompany an abnormal elevation of acetylcholine and partial resistance to acetylcholinesterase inhibitors. To analyze the flow mechanism, we examined another spectra of genes, using carbamylcholine which affects acetylcholine release at the synapse in addition to both nicotinic and muscarinic actions in higher organisms.
Many mutants resistant to levamisole are also resistant to carbachol (Genetics 95 905 '80; Neuroscience 5 967 '80). If the release of acetylcholine is facilitated by mutations, a low concentration of carbachol may cause an animal to fall into a hypersensitive state. From EMS- treated F2 ,we isolated 23 independent mutants potentially hypersensitive to a low concentration of carbachol. Five strains are lethal and the remaining severely paralyzed by 1 mM carbachol. Most strains isolated were hypercontracted but two strains showed nearly normal and locomotion in the absence of carbachol. Along with the progress of pharmacological and genetic analyses using these strains, we are performing an in vitro biochemical assay of the transmitter release.