부산대학교 도서관

Previous electrophysiological studies on the early-evolved metazoan Hydra vulgaris provided evidence that glutamate, acting through a-amino-3-hydroxy-5-meth- yl-4-isoxazolepropionic acid (AMPA) and kainate receptors, affects hydra's pacemaker systems; immunocytochemical studies showed that N-methyl-n-aspartate (NMDA) receptors were present in hydra tentacles; behavioral studies demonstrated that NMDA/n-serine affected mouth opening induced by reduced glutathione, and with AMPA/kainate, discharge of nematocysts. In this study, extracellular recordings were made from the tentacle and peduncle of hydra during bath application of NMDA and D-serrne (both at 1 × 10-5 mol-1 to 1 × 10-9 mol 1-1) in the presence of 1 × 10-7 mol 1-1 AMPA or kainate. NMDA/D-serine produced a significant increase in tentacle activity, increasing the rate of tentacle pacemaker pulses (TPs) at 1 × 10-7 mol 1-1, and small, behaviorally uncorrelated tentacle pulses (SUTPs) at 1 × 10-5 mol 1-1. The NMDA antagonist, D-2-amino-5- phosphonopentanoic acid (D-AP5), counteracted the effects. NMDA/D-serine (1 × 10-7 moL 1-1) also caused a potentially significant (trend) decrease in the rate of small, behaviorally uncorrelated electrical body pulses (SUBPs) and rhythmic potentials (RPs). The effect was counteracted by D-AP5. The ectodermal contraction burst (CB) pace- maker system was unaffected by NMDA/D-serine. Our results indicate that glutamate, acting on NMDA/AMPA- kainate receptors, may cause opposing effects on the coordinating systems of tentacle and body-exciting the tentacle effectors and potentially causing an inhibition in the body column. [ABSTRACT FROM AUTHOR]