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The Journal of Neurophysiology Vol. 82 No. 3 September 1999, pp. 1647-1650
Copyright ©1999 by the American Physiological Society
RAPID COMMUNICATION
Department of Physiology, University of Munich, D-80336 Munich, Germany
Takigawa, Tomoko and
Christian Alzheimer.
Variance Analysis of Current Fluctuations of Adenosine- and
Baclofen-Activated GIRK Channels in Dissociated Neocortical Pyramidal
Cells. J. Neurophysiol. 82: 1647-1650, 1999. Whole cell recordings were obtained from pyramidal cell
somata acutely isolated from rat neocortex. In voltage-clamp mode, adenosine (0.3-1000 µM), and the GABAB receptor agonist,
baclofen (1-300 µM), induced K+ current responses
mediated by G protein-activated inwardly rectifying K+
(GIRK) channels. In our preparation, adenosine activated GIRK currents
with an average EC50 of 2 µM. Baclofen had an average EC50 of 26 µM. To estimate and compare unitary
conductance and density of GIRK channels activated by either adenosine
or baclofen, we performed variance analysis of current fluctuations
associated with the application of the two agonists at increasing
concentrations. Irrespective of the agonist tested, GIRK channels
displayed an average single-channel conductance of 25 pS at our
recording conditions ([K+]o: 60 mM). Assuming
that GIRK channel conductance increases in proportion to the square
root of [K+]o, this would translate into 5-6
pS at physiological ion gradients. GIRK channels activated by adenosine
or baclofen were not only identical in terms of unitary conductance,
they also displayed the same average density of 0.5 channels
µm
2 for both agonists. Our data strongly suggest that
the two compounds recruit the same type of channel and thus most likely
share a common transduction and effector system.
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