NMDA and GABAB receptors are involved in controlling nematocyst discharge in hydra

The role of chemical neurotransmission in nematocyst discharge was investigated by stimulating the cnidocils of nematocysts in ablated tentacles of Hydra vulgaris with a piezoelectrically-driven glass probe, in the presence of selected neurotransmitters. Acetylcholine, dopamine, epinephrine, glycine, and serotonin (10− 4, 10− 6, 10− 8 M) per se, did not alter stenotele and desmoneme discharge. γ-Amino-butyric acid (GABA) significantly increased desmoneme discharge when the cnidocil of another desmoneme in the same or adjacent battery cell complex was stimulated without affecting the discharge rates of the directly stimulated desmonemes or stenoteles. Baclofen (GABAB agonist) mimicked the increase; its antagonist, phaclofen, counteracted it. GABAA agonists and antagonists did not alter discharge rates. Glutamate caused a dose-dependent increase in the discharge rate of directly stimulated stenoteles; distant stenotele and desmoneme discharge rates were unaffected. Kainate, AMPA, and NMDA, per se, did not alter discharge rates. Co-administration of NMDA and kainate mimicked glutamate's effects. AMPA plus NMDA increased discharge rates. DAP-5 (NMDA antagonist) and CNQX, (kainate/AMPA antagonist) counteracted the increase. The findings suggest that metabotropic GABA is involved in recruiting desmonemes by disinhibiting those previously inhibited, and that the NMDA/kainate–AMPA mechanism regulating Ca++ entry in higher neuroeffector systems is an early-evolved process, which, in hydra, modulates nematocyst discharge.