HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Correction (v502,p715) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chiesa, N Articles by Wanke, E Search for Related Content PubMed PubMed Citation Articles by Chiesa, N Articles by Wanke, E

Department of General Physiology and Biochemistry, University of Milano, Italy.

1. The regular firing of a Hodgkin-Huxley neurone endowed with fast Na+ and delayed K+ channels can be converted into adapting firing by appending HERG (human eag-related gene) channels. 2. The computer model predictions were verified by studying the firing properties of F-11 DRG neurone x neuroblastoma hybrid cells induced to differentiate by long-term exposure to retinoic acid. These cells, which express HERG currents (IHERG), show clear spike-frequency adaptation of their firing when current clamped with long depolarizations. 3. In agreement with the prediction, the selective blocking of IHERG by class III antiarrhythmic drugs always led to the disappearance of the spike-frequency adaptation, and the conversion of adapting firing to regular firing. 4. It is proposed that, in addition to their role in the repolarization of the heart action potential, HERG channels may sustain a process of spike-frequency adaptation, and hence contribute to the control of burst duration in a way that is similar to that of the K+ currents, IAHP, IC and IM. In addition to the known cardiac arrhythmia syndrome (LQT2), genetic mutations or an altered HERG expression could lead to continuous hyperexcitable states sustained by the inability of nerve or endocrine cells to accommodate to repetitive stimuli. This might help in clarifying the pathogenesis of still undefined idiopathic familial epilepsies.

This article has been cited by other articles:

				Y. Zhu, C. M. Golden, J. Ye, X.-Y. Wang, H. I. Akbarali, and J. D. Huizinga ERG K+ currents regulate pacemaker activity in ICC Am J Physiol Gastrointest Liver Physiol, December 1, 2003; 285(6): G1249 - G1258. [Abstract] [Full Text] [PDF]

				T. Sacco, A. Bruno, E. Wanke, and F. Tempia Functional Roles of an ERG Current Isolated in Cerebellar Purkinje Neurons J Neurophysiol, September 1, 2003; 90(3): 1817 - 1828. [Abstract] [Full Text] [PDF]

				F. S. Cayabyab, F. W. L. Tsui, and L. C. Schlichter Modulation of the ERG K+ Current by the Tyrosine Phosphatase, SHP-1 J. Biol. Chem., December 6, 2002; 277(50): 48130 - 48138. [Abstract] [Full Text] [PDF]

				G. A. M. Smith, H.-W. Tsui, E. W. Newell, X. Jiang, X.-P. Zhu, F. W. L. Tsui, and L. C. Schlichter Functional Up-regulation of HERG K+ Channels in Neoplastic Hematopoietic Cells J. Biol. Chem., May 17, 2002; 277(21): 18528 - 18534. [Abstract] [Full Text] [PDF]

				F. S. Cayabyab and L. C. Schlichter Regulation of an ERG K+ Current by Src Tyrosine Kinase J. Biol. Chem., April 12, 2002; 277(16): 13673 - 13681. [Abstract] [Full Text] [PDF]