Effects of GABAB ligands on the GSH-induced electrical activity of the hypostome in hydra

Reduced glutathione, GSH, artificially induces the signature feeding behavior in the early-evolved metazoan, Hydra vulgaris. Evidence has shown that the mouth opening response is prolonged by the inhibitory neurotransmitter, GABA. By making extracellular recordings of a detached reduced-tentacle hypostome, it is possible to record the electrical activity produced by GSH and to observe the effects of the inhibitory neurotransmitter, gamma-amino-butyric acid (GABA), the GABAB agonist (baclofen) and the GABAB antagonist, (phaclofen). When an electrode is placed on the mouth of the hypostome, thus blocking the mouth opening, and the ligands are placed in the bath surrounding the base of the hypostome, the following effects are observed: GSH increased small-uncorrelated hypostomal pulses (SUHPs), medium-uncorrelated hypostomal pulses (MUHPs), pacemaker bursting pulses (PBPs) and pulses per pacemaker bursting pulse (P/PBPs). Although GABA per se produced no effect when administered with GSH, baclofen caused an increase in SUHPs, while phaclofen per se caused a decrease; coadministration of baclofen and phaclofen mutually cancelled their individual effects. This suggests that at least some of the SUHPs might be GSH neuronal impulses having metabotropic (GABAB) receptor involvement. GSH coadministered with baclofen and phaclofen caused a decrease in MUHPs and rhythmic potentials (RPs); GABA administered with GSH produced no effect on MUHPs and RPs. When the ligands were placed within the pipette at the mouth (exposing the mouth opening to ligands and blocking the proximal portion of the hypostome), the following effects were observed: GSH increased MUHPs and decreased extra-large uncorrelated hypostomal pulses (XLUHPs) and P/PBPs; this comports with the previously observed GSH induced cone-formation of the hypostome, now hypothesized to be reflected in the increase MUHPs (which may be muscle pulses) and the concurrent inhibition of body contraction (considered to be mediated by XLUHPs and PBPs). This effect was abolished by GABA, which increased the frequency of the large pulses, but not mimicked by baclofen nor counteracted by phaclofen, both of which also decreased in the large pulses. This suggests that GABA inhibition of GSH activity might also involve the action of GABA on its ionotropic receptors and that GABAB receptors exist on the excitatory effector circuits. GSH administered with baclofen caused a decrease in SUHPs. In general, GSH administered alone, GSH and GABA, GSH and phaclofen, GSH and baclofen and GSH coadministered with baclofen and phaclofen caused significantly increased activity when applied directly to the apex of the hypostome, indicating that both GSH and GABAB receptors are concentrated in or around the hypostomal apex. Although GABA combined with GSH produced no significant differences in the frequency of any of the parameters measured in the bath-applied method, coadministration increased LUHPs, XLUHPs, PBPs and RPs in the pipette-applied method—suggesting prolongation of mouth opening. The results support the behavioral observations that GABA inhibits the cessation of the GSH-induced feeding response and indicates that GSH and GABA receptors are differentially distributed in the hypostome