The KCNQ2 potassium channel: splice variants, functional and developmental expression. Brain localization and comparison with KCNQ3.

Abstract:

:Benign familial neonatal convulsions, an autosomal dominant epilepsy of newborns, are linked to mutations affecting two six-transmembrane potassium channels, KCNQ2 and KCNQ3. We isolated four splice variants of KCNQ2 in human brain. Two forms generate, after transient expression in COS cells, a potassium-selective current similar to the KCNQ1 current. L-735,821, a benzodiazepine molecule which inhibits the KCNQ1 channel activity (EC50 = 0.08 microM), also blocks KCNQ2 currents (EC50 = 1.5 microM). Using in situ hybridization, KCNQ2 and KCNQ3 have been localized within the central nervous system, in which they are expressed in the same areas, mainly in the hippocampus, the neocortex and the cerebellar cortex. During brain development, KCNQ3 is expressed later than KCNQ2.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Tinel N,Lauritzen I,Chouabe C,Lazdunski M,Borsotto M

doi

10.1016/s0014-5793(98)01296-4

subject

Has Abstract

pub_date

1998-11-06 00:00:00

pages

171-6

issue

3

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(98)01296-4

journal_volume

438

pub_type

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