title: Regulation of acetylcholine receptors on chick ciliary ganglion neurons by components from the synaptic target tissue.
abstract: Chick ciliary ganglion neurons have nicotinic acetylcholine receptors (AChRs) that mediate synaptic transmission through the ganglion. A soluble component of about 50 kDa from embryonic eye tissue, the synaptic target of the ganglion, increases the development of ACh sensitivity by the neurons 10-fold over a 1-week period in culture. The increased sensitivity does not arise from a change in agonist affinity or esterase activity. Both the basal ACh response obtained in the absence of the 50-kDa component and the elevated responses obtained with it can be inhibited by neuronal bungarotoxin (nBgt) but not by alpha-bungarotoxin (alpha Bgt). Increases of less than twofold are observed for the binding of anti-AChR monoclonal antibody 35 (mAb 35), nBgt, and alpha Bgt to the neurons under these conditions. Extract fractions containing the 50-kDa component also enable the neurons to enhance their ACh responses through a cAMP-dependent mechanism. Either the 50-kDa fraction induces the appearance of a new type of AChR regulated by cAMP, or it alters the function of existing AChRs. The 50-kDa fraction produces no change in neuronal growth but can increase GABA responses sixfold, indicating that its effects are not confined to AChRs. It is not clear whether a single molecular species is responsible for the diverse regulatory effects or whether several types of active components are present in the fraction. The component which enhances ACh sensitivity is trypsin-sensitive and heat-labile, as expected for a protein. The component may be widely distributed since the 50-kDa fraction from a number of tissues can increase the ACh response. The fraction from eye tissue, however, has a specific activity 5-10 times greater than that of the liver fraction. A wide distribution would suggest multiple targets and roles for the component during development.
authors.affiliation: Department of Biology, University of California, San Diego, La Jolla 92093.
authors.forename: S W
authors.initials: SW
authors.lastname: Halvorsen
authors.forename: H A
authors.initials: HA
authors.lastname: Schmid
authors.forename: A E
authors.initials: AE
authors.lastname: McEachern
authors.forename: D K
authors.initials: DK
authors.lastname: Berg
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001665:Binding Sites; D002038:Bungarotoxins / Q000494:pharmacology; D002478:Cells, Cultured; D002642:Chick Embryo; D000242:Cyclic AMP / Q000494:pharmacology; D005123:Eye / Q000737:chemistry / Q000196:embryology; D005726:Ganglia, Parasympathetic / Q000187:drug effects / Q000196:embryology / Q000502:physiology*; D009414:Nerve Growth Factors / Q000494:pharmacology; D009419:Nerve Tissue Proteins / Q000494:pharmacology; D009474:Neurons / Q000502:physiology*; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology; D011978:Receptors, Nicotinic / Q000502:physiology*; D013569:Synapses / Q000502:physiology*; D013997:Time Factors; D014020:Tissue Extracts / Q000494:pharmacology
chemical_list: D002038:Bungarotoxins; D009414:Nerve Growth Factors; D009419:Nerve Tissue Proteins; D011963:Receptors, GABA-A; D011978:Receptors, Nicotinic; D014020:Tissue Extracts; D000242:Cyclic AMP; D000109:Acetylcholine