Worm Breeder's Gazette 11(2): 87
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.
Recent studies in invertebrate glutamate receptors indicate the presence of at least three types of glutamate receptors, none of which are of the NMDA type. Pharmacological data have shown invertebrate glutamate receptor ion channels have less selectivity for noncompetitive antagonists than that of NMDA receptor ion channels and are not shared a voltage-sensitive block by Mg2+ ions, a property of NMDA receptor ion channel. We have tested pharmacological effect of noncompetitive antagonist of NMDA receptors to the worm. In competition assay using cut worm bathing in drug solution, nicotinic transmission appeared to be specifically antagonized by ketamine, a non-competitive antagonist of NMDA receptor. We have isolated sixteen EMS induced mutants showing convulsions against 30mM ketamine and other NMDA noncompetitive antagonists; 1mM PCP and MK-801. In the case of cut worm assay, convulsion could be induced at less than one tenth concentrations. Genetic study to one strain kh30 identified a gene kra-1 which was mapped on the locus closed to mec-1 and unc-68 loci on chromosome V. kra-1(kh30) animal was weak resistant to nicotine (0.1mM), suggesting this convulsion was derived from defective function of nicotine receptor system. Defective site of kra- 1(kh30) might be on nicotinic receptor-associated ion channel because kra-1(kh30) was also weak resistant to channel activator ouabine (0. 1mM). Competitive nicotinic antagonist d-tubocuraine suppressed ketamine function to kra-1(kh30) animal. This suggests that binding affinity of ketamine to ion channel decreased in inactivated state. Finally, convulsion expression of kra-1(kh30) animal with ketamine was also suppressed by Mg2+ ion. These data permit us to conclude that this ion channel could be associated by nicotinic receptor with pharmacological homology to vertebrate NMDA ion channel. Cloning and molecular study of the gene will confirm a pharmacological results. [See Figure 1]