It is known that norepinephrine-containing neurons in the locus coeruleus fire most frequently during waking, less during non REM sleep, and are virtually silent during and before REM sleep. Based on these observations, Siegel and Rogawks proposed that the silence allows brain norepinephrine receptors to recover from desensitization that results from high activity during the waking periods. If this hypothesis is correct, we should see a global reduction in the number of postsynaptic norepinephrine NE receptors in during prolonged sleep loss in response to increased norepinephrine levels. Few studies have actually found reduced postsynaptic receptor levels. When norepinephrine postsynaptic receptor levels are found to be reduced they are usually accompanied by an increase in affinity, which suggests a compensatory mechanism that would maintain the receptors near normal levels.
Many studies do suggest a catecholamine-enhancing effect of sleep deprivation.
Rats also show behavioral sensitivity to dopamine agonists following REM sleep deprivation, which leads to the hypothesis that modification of sensitivity is due to a hyperactivity of the dopamine system. Pharmacological evidence also suggests increased catecholamine functioning during sleep deprivation based on the findings that sleep deprivation and catecholamine-enhancing drugs, such as amphetamine, Ritalin, and cocaine, have similar neurobiological effects. However, many animal studies do not support a catecholamine-enhancing effect of sleep deprivation. Additionally, the combination of catecholamine depletion with sleep deprivation leads to greater cognitive deficits than either treatment alone. Finally, d ecreases in norepinephrine levels have been reported in the hindbrain , midbrain , hippocampus , and hypothalamus have been reported following REM- or total sleep deprivation.