GABA and glutamate receptors are involved in modulating pacemaker activity in hydra.

The effects of gamma-amino butyric acid (GABA) and glutamate, their ionotropic agonists and antagonists on hydra's ectodermal and endodermal pacemaker systems were studied. GABA decreased ectodermal body contraction bursts (CBs) and the number of pulses in a burst (P/CB) and endodermal rhythmic potentials (RPs); tentacle pulses (TPs) were not affected. The GABA(A) agonist, muscimol, and the benzodiazepine receptor agonist, diazepam, mimicked the effects of GABA on the endodermal system. The GABA(A) antagonist bicuculline counteracted GABA's effects. Low concentrations of glutamate increased CBs and RPs. Higher concentrations required concanavalin A (Con A) to produce the same effect on CBs and P/CB. TPs were increased by high concentrations of glutamate and kainate. The ionotropic glutamate agonist, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) also required Con A to increase CBs and RPs. The effects of AMPA were antagonized by 6-nitro-7-sulfamoylbenzo[f]quinoxaline-2,3-dione (NBQX), which, per se, decreased CBs. The results indicate that GABA and glutamate, acting on their ionotropic receptors, modify the impulses of hydra's pacemaker systems. On the whole GABA decreased the outputs of both ectodermal and endodermal impulse generating systems, while glutamate increased them.