Although, the suprachiasmatic nucleus (SCN) of the hypothalamus acts as the 
central clock in mammals, the circadian expression of clock genes has been 
demonstrated not only in the SCN, but also in peripheral tissues and brain 
regions outside the SCN. However, the physiological roles of extra-SCN circadian 
clocks in the brain remain largely elusive. In response, we generated 
Nkx2.1-Bmal1-/- mice in which Bmal1, an essential clock component, was 
genetically deleted specifically in the ventral forebrain, including the 
preoptic area, nucleus of the diagonal band, and most of the hypothalamus except 
the SCN. In these mice, as expected, PER2::LUC oscillation was drastically 
attenuated in the explants of mediobasal hypothalamus, whereas it was maintained 
in those of the SCN. Although, Nkx2.1-Bmal1-/- mice were rhythmic and nocturnal, 
they showed altered patterns of locomotor activity during the night in a 12:12-h 
light:dark cycle and during subjective night in constant darkness. Control mice 
were more active during the first half than the second half of the dark phase or 
subjective night, whereas Nkx2.1-Bmal1-/- mice showed the opposite pattern of 
locomotor activity. Temporal patterns of sleep-wakefulness and feeding also 
changed accordingly. Such results suggest that along with mechanisms in the SCN, 
local Bmal1-dependent clocks in the ventral forebrain are critical for 
generating precise temporal patterns of circadian behaviors.