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J Neurophysiol 82: 1647-1650, 1999;
0022-3077/99 $5.00
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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

Variance Analysis of Current Fluctuations of Adenosine- and Baclofen-Activated GIRK Channels in Dissociated Neocortical Pyramidal Cells

Tomoko Takigawa and Christian Alzheimer

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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