title: Action of excitatory amino acids on hypodermis and the motornervous system of Ascaris suum: pharmacological evidence for a glutamate transporter.
abstract: Electrophysiological and pharmacological experiments suggest the presence of an electrogenic glutamate transporter in the motornervous system of the parasitic nematode Ascaris suum. This putative transporter occurs in hypodermis (a tissue in some respects analogous to glia) and in DE2 motorneurons, a dorsal excitatory motorneuron class which receives excitatory glutamatergic post-synaptic potentials. Glutamate application to hypodermis produced non-conductance mediated depolarizations that were smaller in amplitude and slower in rate of rise than DE2 responses where a glutamate-activated conductance occurs. The hypodermal response is sodium dependent and calcium independent. Excitatory amino acid ionotropic receptor agonists (kainate, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid and N-methyl-D-aspartate) were ineffective in eliciting hypodermal responses. The ionotropic receptor antagonist, 6,7-dinitroquinoline-2,3-dione, had no effect on hypodermal glutamate responses. The L- and D-form of glutamate, aspartate and homocysteate produced hypodermal and DE2 depolarizations consistent with the pharmacological profile for glutamate transporters in other systems. Glutamate transport inhibitors (L-trans-pyrrolidine-2,4-dicarboxylate and beta-hydroxyaspartate) elicited electrogenic depolarizations in hypodermis and DE2. These results suggest that the hypodermal glutamate response has an electrogenic transporter component, while the DE2 response has 2 components, one conductance-mediated and the other due to an electrogenic transporter.
authors.affiliation: Department of Zoology, University of Wisconsin-Madison 53706, USA. redavis@facstaff.wisc.edu
authors.forename: R E
authors.initials: RE
authors.lastname: Davis
mesh_terms: D018528:ATP-Binding Cassette Transporters / Q000378:metabolism*; D027322:Amino Acid Transport System X-AG; D000818:Animals; D017165:Ascaris suum / Q000187:drug effects / Q000502:physiology*; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004553:Electric Conductivity; D004848:Epithelium / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018846:Excitatory Amino Acids / Q000494:pharmacology*; D018698:Glutamic Acid / Q000378:metabolism* / Q000494:pharmacology; D007608:Kainic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D008839:Microelectrodes; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D011810:Quinoxalines / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism
chemical_list: D018528:ATP-Binding Cassette Transporters; D027322:Amino Acid Transport System X-AG; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018846:Excitatory Amino Acids; D011810:Quinoxalines; C011274:3-hydroxyaspartic acid; D001224:Aspartic Acid; D018698:Glutamic Acid; C020889:dihydrokainic acid; C056723:FG 9041; D012964:Sodium; D007608:Kainic Acid; D002118:Calcium