In REM sleep

Capece, M. L., Baghdoyan, H. A. Lydic, R. (1999). New directions for the study of cholinergic REM sleep generation Specifying presynaptic and postsynaptic mechanisms. In REM Sleep, ed. B. N. Mallick S. Inoue, pp. 123-41. London Narosa Press. 

Velazquez-Moctezuma, J., Shiromani, P. J. 8i Gillin, J. C. (1990b). Acetylcholine and acetylcholine receptor subtypes in REM sleep generation. Prog. Brain Res. 84,... 

The hypothesis of the role of HA in wakefulness stems from the observation that administration of the classical antihistamines (i.e. H3 receptor antagonists) induced sedation. These first-generation antihistamines, used to treat inflammatory reactions, could cross the blood-brain barrier and block the central Hi receptor (White Rumbold, 1988). The first study examining the effect of antihistamines on sleep-wakefulness in cats reported an increase in NREM sleep and a decrease in REM sleep (Jewett, 1968). Similar results were also obtained in dogs (Wauquier et ah, 1981) and humans (Risberg et ah, 1975 Bassano Caille, 1979 Nicholson et ah, 1985 Adam Oswald, 1986). Intraventricular application of HA in the anesthetized rat caused a dose-dependent decrease in the duration of narcosis, whereas intraventricular application of HA in conscious... 

Figure 7.3 Interspike interval (ISI) histograms of midbrain dopamine neural firing in behaving rats (reproduced with permission from (Miller et al. 1983)). Note the nearly identical mean intervals, consistent with reported mean firing rate similarities between SWS and REM sleep, as opposed to the broader ISI range observed in REM sleep, reflective of the burst firing in a significant subpopulation of neurons (contrast the widths of the dashed bars above the histograms).

Albin R., Koeppe R., Chervin R. et al. (2000). Decreased striatal dopaminergic innervation in REM sleep behavior disorder. Neurology. 55, 1410-12. 

Inability to maintain wakefulness bouts Severe decrease in REM sleep latency Frequent cataplexy and direct transitions to REM sleep... 

Mild decrease in REM sleep latency Absence of cataplexy or direct transitions to REM sleep Inability to maintain wakefulness bouts Mild decrease in REM sleep latency Occasional cataplexy and direct transitions to REM sleep Inability to maintain wakefulness bouts Severe decrease in REM sleep latency Frequent cataplexy and direct transitions to REM sleep Inability to maintain wakefulness bouts Severe decrease in REM sleep latency Frequent cataplexy and direct transitions to REM sleep Inability to maintain wakefulness bouts Severe decrease in REM latency Frequent cataplexy and separable direct transitions to REM sleep... 

Characterization of the receptor knockout mice (OXjR / and 0X2R l ) provided important information about the differential roles of the two receptors in both vigilance state control and the symptoms of narcolepsy (Kisanuki et al., 2000 Willie et al., 2003). In contrast to the direct transitions to REM sleep and abrupt behavioral arrests that characterized orexin mice, 0X,R l mice exhibited no direct transitions to REM sleep and only a modest decrease in REM sleep latency (Kisanuki et al, 2000). 0XiR / mice also showed slight fragmentation of vigilance states when compared with the normal animals (Kisanuki et al., 2000). 

This belief was further supported by the evidence of a correlation between the clinical response and REM sleep suppression as well as a temporal relationship between the onset of clinical response and REM sleep suppression. However, some of the later studies suggested that REM sleep suppression is not necessary for the antidepressant action (Gillin 1983). For example, some studies show evidence of no change or even an increase in REM sleep with the treatment of depression (Gillin et al. 2001). Recently, Landolt Gillin (Landolt and Gillin 2002) have also demonstrated that the antidepressant response to phenelzine treatment does not depend on elimination of REM sleep or inhibition of slow wave activity in non-REM sleep. However, the generalization of some of these studies is limited because of their small sample size. 

In rats, cocaine (6 mg/kg, i.p. or p.o.) has been shown to induce a significant increase in sleep latency and a reduction in total sleep time, including a decrease in both non-REM sleep and REM sleep (Schwartz 2004). In humans, cocaine, amphetamines, and methylphenidate also produce decreases in sleepiness, an increased latency to sleep, and a marked decrease in REM sleep associated with an increased latency to the onset of this state. Amphetamine, methylphenidate, and cocaine are known to act by enhancing the amount of the monoamines available within the synaptic cleft of synapses in the CNS. 

Kales J., Allen C., Preston T. A., Tan T. L., Kales A. (1970). Changes in REM sleep and dreaming with cigarette smoking and following withdrawal. Association of Professional Sleep Societies Meeting. Abstracts Book, 7, 347-8. 

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