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Sleep modulation mechanism

Bruxism mainly occurs in stage 2 sleep and REM sleep (Bader et ah, 1977). A relationship to stress and anxiety has been suggested, but the disorder can be chronic without apparent association with stress (Faulkner, 1990 Pierce et ah, 1995). It has been suggested that the central dopaminergic system may be involved in the modulation of sleep bruxism (Lobbezoo et al., 1997). Case reports indicate that bruxism can be induced by the SSRI paroxetine (Romanelli et al., 1996). The mechanism remains unclear possibilities include sleep disturbance, serotonergic-mediated inhibition of dopamine manifesting as akathisia, and SSRI-induced anxiety. SSRI-induced bruxism may respond to therapy with buspirone (Ellison et al., 1993). [Pg.116]

Noradrenergic projections are involved in the modulation of sleep cycles, appetite, mood, and cognition by targeting the thalamus, limbic structures, and cortex. An increase in noradrenergic function appears to convey some of the therapeutic effect of antidepressants, although the exact mechanisms remain poorly understood (Charney, 1998 Anand and Charney, 2000 Frazer, 2000). [Pg.29]

McCance SL, Cohen PR, Cowen PJ Dthium increases 5-HT-mediated prolactin release. Psychopharmacology 99 276-281, 1989 McCann U, Hatzidimitriou G, Ridenour A, et al Dexfenfluramine and serotonin neurotoxicity further prechnical evidence that chnical caution is indicated. J Pharmacol Exp Ther 269 792-798, 1994 McCarley RW REM sleep and depression common neurobiological control mechanisms. Am J Psychiatry 139 565-570, 1982 McCarley RW, Hobson JA Neuronal excitability modulation over the sleep cycle a structural and mathematical model. Science 189 58-60, 1975... [Pg.692]

The PGO waves of REM sleep are epileptiform. Both consist of spike and wave EEG complexes that are morphologically indistinguishable. In both PGO waves and temporal lobe epilepsy, these spike and wave complexes are generated by similar mechanisms owing to a physiological decline in inhibitory modulation (REM sleep) or to structural damage (TEE), neurons are disinhibited and fire in intense bursts, of which the EEG spike and wave complex is the extracellular record. [Pg.196]

Many hormonal secretion processes also exhibit strong circadian components. This is true, for instance, for cortisol, antidiuretic hormone, and growth hormone. The secretion of growth hormone is markedly increased during the early periods of sleep, and the secretion of antidiuretic hormone also reflects the sleep-wake cycle. The mechanisms underlying these oscillations can often be traced back to cyclical variations in the activity of the central nervous system. At the same time, the circadian rhythm modulates the above-mentioned ultradian oscillations. [Pg.34]

Stress is also involved in the modulation of the immune responses through mechanisms involving the neurotransmitter serotonin. This is a biologically active amine that plays a prominent role in the regulation of processes such as mood, appetite and sleep. During neurotransmission, serotonin is released from neurons into the synaptic cleft between cells. The amount of serotonin available for neurotransmission in the synaptic cleft is regulated largely by the serotonin transporter involved in the reuptake of serotonin after it has been released.23... [Pg.123]


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