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gamma‐Aminobutyric acid hyperpolarizes rat hippocampal pyramidal cells through a calcium‐dependent potassium conductance.
Author(s) -
Blaxter T J,
Carlen P L,
Davies M F,
Kujtan P W
Publication year - 1986
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1986.sp016041
Subject(s) - picrotoxin , depolarization , hyperpolarization (physics) , reversal potential , membrane potential , chemistry , biophysics , hippocampal formation , resting potential , conductance , slice preparation , gamma aminobutyric acid , neuroscience , calcium , electrophysiology , patch clamp , gabaa receptor , biology , biochemistry , stereochemistry , physics , receptor , organic chemistry , condensed matter physics , nuclear magnetic resonance spectroscopy
Application of gamma‐aminobutyric acid (GABA) to the dendrites of CA1 pyramidal cells in hippocampal slices produced depolarizing and hyperpolarizing responses. Picrotoxin (50 microM) blocked the depolarizing response of the dendrites to GABA but not the hyperpolarizing responses of the dendrites. The hyperpolarizing response of the cell body to GABA was reduced but not blocked by picrotoxin, suggesting the presence of a complex response at the cell body. The depolarizing response of the dendrites and the hyperpolarizing response of the cell body appeared to be at least partly Cl‐ dependent as they were respectively increased and decreased in size in low‐Cl‐ artificial cerebrospinal fluid (ACSF), while the hyperpolarizing response of the dendrites was unaffected. The hyperpolarizing response of the dendrites was increased in amplitude in low‐K+ ACSF and the extrapolated reversal potential of the response became more negative, suggesting that the response was K+ dependent. The hyperpolarizing response of the dendrites was decreased in size in high‐K+ ACSF and could be readily inverted by current injection. The reversal potential became less negative in high‐K+ ACSF in a similar manner to that of the slow after‐hyperpolarization following a train of spikes, indicating that the response was a K+ conductance. Perfusion of the slice with normal or 0‐Ca2+ ACSF containing Cd2+ or Mn2+ blocked synaptic transmission, increased spike duration and blocked the slow phase of the spike after‐hyperpolarization (a.h.p.). This latter potential is thought to be mediated by a Ca2+‐dependent K+ conductance. Later, the hyperpolarizing response of the dendrites to GABA was blocked without an effect on the other GABA responses. Pressure application of Cd2+ (0.2‐2 mM) onto the surface of the slice rapidly reduced or blocked the slow a.h.p. and the dendritic hyperpolarizing response to GABA. Intracellular injection of EGTA rapidly blocked the slow phase of the a.h.p. and then later blocked or reduced the dendritic hyperpolarizing response to GABA. We conclude that the hyperpolarizing response of the dendrites to GABA is mediated by a Ca2+‐dependent K+ conductance.