Glutamatergic and GABAnergic control in the tentacle effector systems of Hydra vulgaris

In addition to their role in orchestrating body and tentacle contractions, hydra\u27s nerves control the behavior of nematocysts; precisely how is still a work in progress. There are strong indications that the classical neurotransmitters, glutamate and GABA (γ-amino-butyric acid), play an essential role in effecting stenotele and desmoneme discharge. In experiments on isolated tentacles of Hydra vulgaris, in which cnidocils were mechanically deflected with a piezo-electrically-driven glass micropipette, stenoteles and desmonemes respond to differences in applied force in a dose-dependent manner. GABA, working through its metabotropic receptor, appears to be involved with the recruitment of desmonemes. Desmonemes in distant battery cells or in another part of a given battery cell were discharged by stimulating a desmoneme cnidocil in the presence of bath-applied GABA or its metabotropic agonist, baclofen. The effect was blocked by phaclofen, its metabotropic antagonist. Neither GABA nor baclofen affected stenotele discharge. GABAA agonists had no effect on nematocyst discharge. Glutamate caused a significant increase in number of stenoteles responding to direct mechanical stimuli, but did not effect desmoneme discharge. The effect was mimicked by NMDA (n-methyl-D-aspartate) together with kainate, or by NMDA plus AMPA (amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid), but not with any ionotropic agonist alone. The effect was blocked by D-AP 5 (D- (-)-2-amino-5-phosphopentanoic acid), a specific NMDA antagonist, or CNQX (6-cyano-7-nitroquinoxaline-2,3-dione), a specific kainate/AMPA antagonist. A glutamatergic mechanism working through ionotropic glutamate receptors appears to lower the firing threshold of stenoteles, perhaps by permitting the entry of Ca2+ into the cell through the early evolved NMDA/kainite/ AMPA mechanism