There is a strong corrolation between CL firing and wakefulness levels. LC neural activity is highest during wakefulness, progressively lower during non-rapid eye movement (REM) sleep, and nearly absent during REM sleep<ref>Aston-Jones G, Bloom FE (1981) Activity of norepinephrine-containing locus coeruleus neurons in behaving rats anticipates fluctuations in the sleep-waking cycle. J Neurosci 1:876–886.</ref>. A more causal finidngs were astablished when inhibiton and stimulation of LC by drugs were mediated to the LC, and that changed the levels of wakefulness<ref>Berridge CW, Foote SL (1991) Effects of locus coeruleus activation on electroencephalographic activity in neocortex and hippocampus. J Neurosci 11:3135–3145.</ref><ref>Berridge CW, Waterhouse BD (2003) The locus coeruleus-noradrenergic system: modulation of behavioral state and state-dependent cognitive processes. Brain Res Brain Res Rev 42:33–84.</ref>. but both the drugs and current may spread beyond the LC to other structures in the dorsolateral pons that may also play important roles in arousal and wake–sleep control, such as the parabrachial nucleus and the preceruleus region<ref>Lu J, Jhou TC, Saper CB (2006) Identification of wake-active dopaminergic neurons in the ventral periaqueductal gray matter. J Neurosci 26:193–202.</ref>. Chemical or genetic lesions limited to the LC produce only small effects on the amount or timing of wakefulness. The role of the LC in arousal remains unclear. ([http://www.jneurosci.org/content/30/43/14543.full source])