An investigation of the pharmacology and underlying mechanism of the responses to gamma-amino butyric acid and ethylenediamine of pyramidal neurones in the hippocampal slice preparation

Abstract

1. Hippocampal pyramidal neurones were successfully maintained in vitro in brain slices. 2. Stable intracellular recordings were made from pyramidal neurones in the CAl region of the pyramidal neurone layer. 3. The iontophoresis of acetylcholine, glutamate, GABA and ethylenediamine produced responses when applied to the dendrites and when applied to the cell body of pyramidal neurones. 4. Ethylenediamine may have acted indirectly on GABA receptors. 5. The depolarizing response of the pyramidal neurone dendrites to GABA was dependent on chloride ions and was also probably dependent on sodium ions. 6. The hyperpolarizing response of the pyramidal neurone dendrites to GABA and ethylenediamine was dependent on potassium ions. 7. The hyperpolarizing response of the pyramidal neurone cell body to GABA and ethylenediamine was dependent on potassium ions. 8. Bicuculline reduced the depolarizing response of the dendrites to GABA and ethylenediamine and reduced the hyperpolarizing response of the cell body to GABA. 9. Picrotoxin reduced the depolarizing response of the dendrites to GABA and ethylenediamine. 10. The hyperpolarizing response of the dendrites to GABA and ethylenediamine was not mediated by the usual bicuculllne-and picrotoxin-sensitive receptor. 11. Benzodiazepines had variable effects on the depolarizing response of the dendrites to GABA or ethylenedlamine and variable effects on the hyperpolarizing response of the cell body to GABA or ethylenediamine. Benzodiazepines had no effect on the hyperpolarizing response of the dendrites to EDA. 12. The hyperpolarizing response of the dendrites to GABA and ethylenediamine was distinct from the hyperpolarizing response of the cell body to GABA and ethylenediamine.