Glutamatergic transmission in hydra: NMDA/D-serine affects the electrical activity of the body and tentacles of Hydra vulgaris (Cnidaria, Hydrozoa).

Previous electrophysiological studies on the early-evolved metazoan Hydra vulgaris provided evidence that glutamate, acting through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainate receptors, affects hydra's pacemaker systems; immunocytochemical studies showed that N-methyl-d-aspartate (NMDA) receptors were present in hydra tentacles; behavioral studies demonstrated that NMDA/d-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-serine (both at 1 x 10(-5) mol l(-1) to 1 x 10(-9) mol l(-1)) in the presence of 1 x 10(-7) mol l(-1) AMPA or kainate. NMDA/d-serine produced a significant increase in tentacle activity, increasing the rate of tentacle pacemaker pulses (TPs) at 1 x 10(-7) mol l(-1), and small, behaviorally uncorrelated tentacle pulses (SUTPs) at 1 x 10(-5) mol l(-1). The NMDA antagonist, d-2-amino-5-phosphonopentanoic acid (D-AP5), counteracted the effects. NMDA/d-serine (1 x 10(-7) mol l(-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) pacemaker 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.