A study of the interactions between glutamate and aspartate at the lobster neuromuscular junction.

The depolarization produced by bath-applied or iontophoretically applied glutamate and aspartate were recorded from lobster muscle fibres by means of intracellular microelectrodes. 2 Bath-applied glutamate or aspartate evoked reversible, membrane depolarizations; however, responses to repeated applications of aspartate decreased progressively in amplitude until a plateau level was attained. Repeated applications of glutamate, kainate, domoate or quisqualate did not produce a similar effect. 3 After a dose of glutamate, responses to bath-applied aspartate were enhanced. Responses to other depolarizing agonists were little affected by previous administration of glutamate. Aspartate dose-depolarization curves were therefore constructed after initial aspartate responses had stabilized. The log-log transforms of the aspartate and glutamate curves had limiting slopes of 0.8 and 2.1 respectively. 4 Iontophoretic application of aspartate to single glutamate-sensitive sites produced small depolarizations with slow time course, compared with the glutamate potentials. When aspartate and glutamate were pulsed simultaneously from a twin-barrelled pipette, the resultant glutamate potential was enhanced. It is suggested that this potentiation was due to summation of agonist concentrations in the receptor region interacting with a second-order dose-response relationship. 5 Bath-applied aspartate increased the amplitude and prolonged the half-decay time of the glutamate potential. This effect was particularly noticeable when the glutamate potential was of slow time course. 6 It is proposed that bath-applied aspartate has an agonist effect whose magnitude is possibly exaggerated by concomitant release of glutamate and/or inhibition by glutamate of aspartate uptake. This agonist action of aspartate is thought to be exerted mainly on extrajunctional areas of the glutamate-sensitive sites.