THE ACTION OF GAMMA-AMINOBUTYRIC ACID (GABA) AND ETHYLENEDIAMINE (EDA) ON LIMULUS AND HELIX CENTRAL NEURONS AND RAT CEREBELLAR AND SYMPATHETIC-GANGLION NEURONS

Intracellular recordings were made from central Limulus and Helix neurons and extracellular recordings from rat cerebellar Purkinje cells and sympathetic ganglia. The actions of .gamma.-aminobutyric acid (GABA) and ethylenediamine (EDA) and related analogs on these preparations were investigated. On Limulus neurons inhibited by GABA, EDA and piperazine were 81 and 186 times, respectively, less potent than GABA. Both the GABA and EDA events were chloride mediated, having similar reversal potentials and were reversibly antagonized by picrotoxinin. The EDA response persisted in high Mg Ringer. On Helix neurons inhibited by GABA, EDA was 92 times less potent while on neurons excited by GABA. EDA was 9.25 times less potent. The other analogs tested had little or no GABA-like effect on either preparation. On rat cerebellar Purkinje cells, EDA was eqipotent with GABA and both compounds were antagonized by bicuculline. Flurazepam only potentiated the action of EDA on 3 out of 23 cells tested while the GABA response of all 23 cells was potentiated by the benzodiazepine. Diaminopropionic acid was a weak inhibitor of cerebellar Purkinje cell firing but flurazepam potentiated this response in 6 out of 10 cells tested. On rat cervical ganglion neurons, EDA was half the potency of GABA and likewise the other analogs were less potent than GABA as depolarizing agents. Incubation with glutamic acid decarboxylase inhibitors had no effect on the EDA response. Cross desensitization between GABA and EDA was demonstrated using the ganglion preparation. This paper suggests that EDA is acting directly to activate at least part of the GABA receptor although the benzodiazepine receptors do not appear to be directly linked to the EDA component of the GABA receptor.