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ACTIONS OF GABA AND ETHYLENEDIAMINE ON CA1 PYRAMIDAL NEURONES OF THE RAT HIPPOCAMPUS
Author(s) -
Blaxter T. J.,
Cottrell G. A.
Publication year - 1985
Publication title -
quarterly journal of experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0144-8757
DOI - 10.1113/expphysiol.1985.sp002898
Subject(s) - picrotoxin , depolarization , hyperpolarization (physics) , bicuculline , reversal potential , chemistry , neuroscience , biophysics , hippocampus , membrane potential , endocrinology , medicine , electrophysiology , gabaa receptor , biology , biochemistry , patch clamp , stereochemistry , receptor , nuclear magnetic resonance spectroscopy
The effects of locally applied γ‐aminobutyric acid (GABA) and ethylenediamine were examined and compared on CA1 pyramidal neurones in slice preparations of rat hippocampus using intracellular voltage recording techniques. Each substance produced both depolarization and hyperpolarization of the dendrites; the cell body responded with hyperpolarization alone. Ion substitution experiments suggest that the depolarizing responses of the dendrites were Cl − dependent and the hyperpolarizing responses of the cell body were dependent on Cl − , which suggests that the Cl − potential ( E Cl ) is different in the dendrites compared with the cell body. The hyperpolarizing responses of the dendrites were dependent on K + . Dendritic depolarizing responses to GABA and ethylenediamine were antagonized by bicuculline and picrotoxin whereas the dendritic hyperpolarizing response was unaffected. The hyperpolarizing responses of the cell body were more difficult to study but it appeared that they were reduced by both bicuculline and picrotoxin. The benzodiazepines flurazepam and diazepam potentiated the dendritic depolarizing responses to GABA and ethylenediamine. It also had this effect on the hyperpolarizing response of the cell body but not on the hyperpolarizing response of the dendrites.