ACTION OF EXCITATORY AMINO-ACIDS ON HYPODERMIS AND THE MOTORNERVOUS SYSTEM OF ASCARIS-SUUM - PHARMACOLOGICAL EVIDENCE FOR A GLUTAMATE TRANSPORTER

Electrophysiological and pharmacological experiments suggest the prese nce of an electrogenic glutamate transporter in the motornervous syste m of the parasitic nematode Ascaris suum. This putative transporter oc curs in hypodermis (a tissue in some respects analogous to glia) and i n DE2 motorneurons, a dorsal excitatory motorneuron class which receiv es excitatory glutamatergic post-synaptic potentials. Glutamate applic ation to hypodermis produced non-conductance mediated depolarizations that were smaller in amplitude and slower in rate of rise than DE2 res ponses 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-m ethyl-4-isoxazole acid and N-methyl-D-aspartate) were ineffective in e liciting hypodermal responses. The ionotropic receptor antagonist, 6,7 -dinitroquinoline-2,3 -dione, had no effect on hypodermal glutamate re sponses. The L-and D-forms of glutamate, aspartate and homocysteate pr oduced hypodermal and DE2 depolarizations consistent with the pharmaco logical 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 electro genic transporter.