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

Document Type

Article

Date of Original Version

4-1-2009

Abstract

Previous electrophysiological studies on the early-evolved metazoan Hydra vulgaris provided evidence that glutamate, acting through α-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 × 10 -5 mol 1 -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- © 2009 Marine Biological Laboratory.

Publication Title, e.g., Journal

Biological Bulletin

Volume

216

Issue

2

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