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 Lettjournal_title
FEBS lettersauthors
Tinel N,Lauritzen I,Chouabe C,Lazdunski M,Borsotto Mdoi
10.1016/s0014-5793(98)01296-4subject
Has Abstractpub_date
1998-11-06 00:00:00pages
171-6issue
3eissn
0014-5793issn
1873-3468pii
S0014-5793(98)01296-4journal_volume
438pub_type
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