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J Neurophysiol 89: 2238-2244, 2003. First published November 27, 2002; doi:10.1152/jn.00957.2002
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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

Interplay Between Activation of GIRK Current and Deactivation of Ih Modifies Temporal Integration of Excitatory Input in CA1 Pyramidal Cells

Tomoko Takigawa and Christian Alzheimer

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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