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The Role of Endogenous Sleep-promoting Substances
Published in Clete A. Kushida, Sleep Deprivation, 2004
Ferenc Obal, Fabio Garcia-Garcia, James M. Krueger
In the suprachiasmatic and paraventricular nuclei VIP immunoreactivity increases during the dark period, when rodents are mostly awake, and decreases during the subsequent light period, when most of the time is spent in sleep (141,142). In addition, VIP immunoreactivity exhibits diurnal variations in the locus ceruleus nucleus and the periaqueductal gray matter. REM sleep deprivation upregulates VIP receptors in the brainstem areas that are involved in the generation and maintenance of REM sleep (143). The injection of VIP into areas of the brain involved with REM sleep generation induces prolonged increases in REM sleep (144). Thus, the oral pontine reticular nucleus (PnO) may be a target for the induction of REM sleep by VIP. VIP often colocalizes with acetylcholine (145,146). The injection of VIP into the PnO in combination with atropine, a cholinergic muscarinic antagonist, prevents VIP-induced REM-sleep increases (147). Injection of VIP into the medial pontine reticular formation (mPRF) of rats also induces REM sleep (148). Microinjection of cholinergic agonists within the mPRF produces a state that is behaviorally indistinguishable from natural REM sleep (114). These findings suggest that VIP promotes REM sleep via brainstem cholinergic mechanisms. However, VIP administered in combination with atropine in PCPA-treated insomniac cats induces an increase in total-time REM sleep (149), suggesting that the effects of VIP on REM sleep are not dependent on cholinergic mechanisms. Intrahypothalamic VIP is a physiological PRL-releasing hormone (150) and may also stimulate intrahypothalamic PRL synthesis (151).
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
Behavioural state control was once thought to be a passive process. However, in 1990 Steriade & McCarley proposed a reciprocal interaction model: an active model of behavioural state control, based on mathematical assumptions about two types of neurons, REM-off and REM-on. As REM-off neurons gradually increased their firing, they would activate REM-on neurons by a feed-forward mechanism. The increase in firing of REM-on neurons would precipitate REM sleep and inhibit the REM-off neurons. As activity in the REM-off group subsided, there would be less activation of REM-on neurons and the balance of activity would switch back to REM-off neurons. This model has subsequently been applied to neurons located in the reticular formation, which have state-dependent firing patterns, that is, consistently changing in relation to the behavioural state of the animal. REM-on neurons include the cholinergic neurons in the PEDUNCULOPONTINE TEGMENTAL NUCLEUS and LATERODORSAL TEGMENTAL NUCLEUS, and the GLUTAMATE- and GLYCINE-containing neurons in the medial pontine reticular formation. REM-off neurons include the SEROTONIN neurons in the RAPHE NUCLEI and the NORADRENALINE neurons in the LOCUS COERULEUS. It has been possible to confirm the connections between these nuclei through the technique of TRACT TRACERS. In addition, in most instances, the RECEPTOR subtypes and excitatory or inhibitory relationships which occur between the nuclei have been ascertained by in vitro electrophysiological recordings. However, the model is still being developed and modified: one particular point which has not been reconciled with the known anatomy and electrophysiology is that these neuronal groups are all active at once during the waking state.
An update on the utility and safety of cholinesterase inhibitors for the treatment of Alzheimer’s disease
Published in Expert Opinion on Drug Safety, 2020
Andrea Haake, Kevin Nguyen, Lauren Friedman, Binu Chakkamparambil, George T Grossberg
In addition to GI side-effects, other commonly reported side effects include: agitation, fatigue, dizziness, headache, influenza-like symptoms and sleep disturbances (Table 1). When compared to placebo, insomnia and vivid dreams are more often cited following donepezil administration, particularly with nighttime dosing [24]. It has been hypothesized that these nighttime symptoms are related to the drug’s mechanism of increasing cholinergic activity, as the REM-induction region within the medial pontine reticular formation is activated by cholinergic transmission [24,30]. Advising patients to take their medication in the morning and spacing out doses immediately before titrating to a higher dose may help alleviate sleep disturbances.