K-ATP channels are K+ channels whose activity is inhibited by the pres
ence of and enhanced by the absence of cytosolic ATP. This property al
lows K-ATP channels to sense cellular intermediary metabolism and dire
ctly couple this information to the modulation of membrane excitabilit
y. Indeed, recent studies from our laboratory and others have suggeste
d that activation of K-ATP channels during anoxia is important in the
response and adaptation of central neurons to hypoxia. In order to ide
ntify K-ATP channels from human brain, we performed a polymerase chain
reaction (PCR) using human cerebral cortex mRNA and primers derived f
rom the ROMK1 sequence, a cDNA clone encoding an ATP-regulated potassi
um channel, recently isolated from rat kidney. We thus identified a no
vel 308-bp PCR product, pKCNJ1, whose expression was found to be restr
icted to a 3.0-kb band in the kidney by probing a human multiple tissu
e northern blot. pKCNJ1 was then used to isolate genomic clones and, u
sing fluorescence in situ hybridization (FISH) to human metaphase chro
mosomes, was mapped to chromosome 11q.