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This Article Full Text Full Text (PDF) All Versions of this Article: 95/5/3073    most recent 00922.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Rateau, Y. Articles by Ropert, N. Search for Related Content PubMed PubMed Citation Articles by Rateau, Y. Articles by Ropert, N.

Expression of a Functional Hyperpolarization-Activated Current (I_h) in the Mouse Nucleus Reticularis Thalami

Laboratoire de Neurophysiologie et Nouvelles Microscopies, Institut National de la Santé et de la Recherche Médicale U603; Centre Nationale de la Recherche Scientifique FRE2500; Ecole Supérieure de Physique et de Chimie Industrielles; and Université Paris Descartes, Paris, France

Submitted 2 September 2005; accepted in final form 13 January 2006

The GABAergic neurons of the nucleus reticularis thalami (nRT) express the type 2 hyperpolarization-activated cAMP-sensitive (HCN2) subunit mRNA, but surprisingly, they were reported to lack the hyperpolarization-activated (I_h) current carried by this subunit. Using the voltage-clamp recordings in the thalamocortical slice preparation of the newborn and juvenile mice (P6–P23), we demonstrate that, in the presence of 1 mM barium (Ba²⁺), the nRT neurons express a slow hyperpolarization-activated inward current, suggesting that the I_h is present but masked in control conditions by K⁺ leak currents. We investigate the identity of the hyperpolarization-activated current in the nRT by studying its physiological and pharmacological profile in presence of Ba²⁺. We show that it has voltage- and time-dependent properties typical of the I_h, that it is blocked by cesium and ZD7288, two blockers of the I_h, and that it is carried both by the K⁺ and Na⁺ ions. We could also alter the gating characteristics of the hyperpolarization-activated current in the nRT by adding a nonhydrolysable analogue of cAMP to the pipette solution. Finally, using the current-clamp recording, we showed that blocking the hyperpolarization-activated current induced an hyperpolarization correlated with an increase of the R_in of the nRT neurons. In conclusion, our results demonstrate that the nRT neurons express the I_h with slow kinetics similar to those described for the homomeric HCN2 channels, and we show that the I_h of the nRT contributes to the excitability of the nRT neurons in normal conditions.

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