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J Neurophysiol (April 1, 2003). 10.1152/jn.00957.2002
Submitted on Submitted 21 November 2002; accepted in final form 22 November 2002
Department of Physiology, University of Munich, D-80336 Munich, Germany
Takigawa, Tomoko and
Christian Alzheimer.
Interplay Between Activation of GIRK Current and Deactivation of
Ih Modifies Temporal Integration of
Excitatory Input in CA1 Pyramidal Cells. J. Neurophysiol. 89: 2238-2244, 2003. Trains of brief iontophoretic
glutamate pulses were delivered onto the apical dendrites of CA1
pyramidal cells at variable frequencies (3-100 Hz) to examine how the
activation of a G protein-activated, inwardly rectifying
K+ (GIRK) conductance alters the postsynaptic processing of
repetitive excitatory input. Application of the GIRK channel agonist
baclofen (20 µM) reduced the amplitude of individual glutamate-evoked
postsynaptic potentials (GPSPs) and attenuated summation of GPSPs so
that higher stimulus intensities were required to fire the cell.
Notably, GIRK channel activation not only decreased GPSPs, but also
suppressed the subsequent afterhyperpolarization (AHP), which arises
from a transient deactivation of the hyperpolarization-activated cation current (Ih). Voltage-clamp recordings ruled
out a direct modulatory action of baclofen on
Ih. GIRK channel activation alone accounts for AHP suppression, firstly because, with smaller GPSP amplitudes, fewer Ih channels are deactivated, resulting
in a diminished AHP, and secondly because, owing to its progressive
increase in the hyperpolarizing direction, the GIRK conductance shunts
a large portion of the remaining AHP. We provide experimental evidence that the suppression of the Ih-dependent AHP
by GIRK channel activation bears particular significance on the
processing of repetitive excitatory inputs at frequencies at which the
deactivation kinetics of Ih exert a
prominent depressing effect. In functional terms, activation of GIRK
current not only produces a time-independent mitigation of incoming
excitatory input, which results directly from the opening of an
instantaneous K+ conductance, but might also cause a
time-dependent redistribution of synaptic weight within a stimulus
train, which we link to an interplay with the deactivation of
Ih.
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