I(h) “run-up” in rat neocortical neurons and transiently rat or human HCN1-expressing HEK293 cells.

Arne Battefeld, Claudia Bierwirth, Ying Chuan Li, Lennart Barthel, Tanja Velmans, Ulf Strauss
J. Neurosci. Res.. 2010-08-30; 88(14): 3067-3078
DOI: 10.1002/jnr.22475

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1. J Neurosci Res. 2010 Nov 1;88(14):3067-78. doi: 10.1002/jnr.22475.

I(h) “run-up” in rat neocortical neurons and transiently rat or human
HCN1-expressing HEK293 cells.

Battefeld A(1), Bierwirth C, Li YC, Barthel L, Velmans T, Strauss U.

Author information:
(1)Institute of Cell Biology and Neurobiology, Center for Anatomy,
Charité-Universitätsmedizin Berlin, Berlin, Germany.

Hyperpolarization-activated cyclic nucleotide-gated ion channels (HCN) are key
determinants of CNS functions. Here we describe an increase in
hyperpolarization-activated current (I(h)) at the beginning of whole-cell
recordings in rat layer 5 cortical neurons. For a closer investigation of this
I(h) increase, we overexpressed the predominant layer 5 rat subunit HCN1 in
HEK293 cells. We characterized the resulting I(h) in the cell-attached and
whole-cell configurations. Breaking into whole-cell configuration led to about a
30% enhancement of rat HCN1-mediated I(h) accompanied by a depolarizing shift in
voltage dependence and an accelerated time course of activation. This current
enhancement is not species specific; for human HCN1, the current similarly
increases in amount and kinetics. Although the changes were bound to cytosolic
solution exchange, they were independent of cAMP, ATP, GTP, and the phosphate
group donor phosphocreatine. Together, these data provide a characterization of
heterologous expression of rat HCN1 and suggest that cytosolic contents suppress
I(h). Such a mechanism might constitute a reserve in h-channel function in vivo.

© 2010 Wiley-Liss, Inc.

DOI: 10.1002/jnr.22475
PMID: 20806410 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus