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

The effects of GABA and glutamate, their ionotropic agonists and antagonists on hydra’s ectodermal and endodermal pacemaker systems were studied. GABA decreased ectodermal body contraction-bursts (CB’s) and the number of pulses in a burst (P/CB) and endodermal rhythmic potentials (RP’s); tentacle pulses (TP’s) were not affected. The GABAA agonist, muscimol and the benzodiazapine receptor agonist, diazepam, mimicked the effects of GABA on the endodermal system. The GABAA antagonist, bicuculline, counteracted GABA’s effects. Low concentrations of glutamate increased CB’s, and RP’s. Higher concentrations required Con A to produce the same effect on CB’s and P/CB. TP’s were increased by high concentrations of glutamate and kainate. The ionotropic glutamate agonist, AMPA also required Con A to increase CB’s and RP’s. The effects of AMPA were antagonized by NBQX, which, per se, decreased CB’s. 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.