Biochemical pharmacology of paradoxical sleep.

Abstract

1 The role of noradrenergic cells in the regulation of paradoxical sleep is still controversial, and experimental data have given rise to contradictory interpretations.2 Early investigations focused primarily on chemical neurotransmissions. However, the process of information transmission between cells involves many other factors, and the cell surface is an important site for transduction of messages into modifications of the activity of postsynaptic cells.3 a-adrenoceptors are believed to play an important role in the control of wakefulness and paradoxical sleep. Experimental evidence suggests that physiological modulation of receptor sensitivity, possibly by specific neuro-modulators, may be a key mechanism in synaptic transmission. 4 In the investigation of the mechanisms involved in paradoxical sleep regulation, lesions of the locus coeruleus have given equivocal results. Collateral inhibition, probably mediated by a2-adrenoceptors, appears to be a powerful mechanism. The exact temporal relationship between noradrenergic cell activation and paradoxical sleep production is not established, but 5-HT appears to be involved. Differences between paradoxical sleep and waking may be related to a physiological modulation of a2-adrenoceptor sensitivity.

Sleep disordered breathing in community psychiatric patients

“…Previous studies of sleep disturbance in psychiatric disorders demonstrated disrupted sleep architecture but did not look for the presence or absence of sleep apnoea 1,[19][20][21] . Psychotropic medications improve sleep architecture but more recent studies reflect the growing awareness of the negative impact of psychotropic medication on weight gain and their association with metabolic syndrome 22 .…”

Clonidine Has a Paradoxical Effect on Cyclic Arousal and Sleep Bruxism during NREM Sleep

“…[1][2][3] REM sleep onset appears to be strongly influenced by the adrenergic and noradrenergic systems. 45,46 The neurotransmitters in these systems are implicated in inhibitory mechanisms that mainly involve postsynaptic α 2 -adrenoceptors in the locus coeruleus area of the brainstem. 47 However, clonidine may also activate nonadrenergic neurons in the pontine reticular formation and thereby exert an indirect influence on the GABA-ergic and cholinergic neurons that modulate REM sleep onset.…”