Article date: April 1978
By: A. NISTRI, A. CONSTANI in Volume 62, Issue 4, pages 495-505
The depolarizations produced by bath‐applied or iontophoretically applied glutamate and aspartate were recorded from lobster muscle fibres by means of intracellular microelectrodes.
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.
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.
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.
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.
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.
The depolarizations produced by bath‐applied or iontophoretically applied glutamate and aspartate were recorded from lobster muscle fibres by means of intracellular microelectrodes.
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.
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.
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.
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.
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.
DOI: 10.1111/j.1476-5381.1978.tb07753.x
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