Increased REM sleep in rats selectively bred for cholinergic hyperactivity

Shiromani, P J; Overstreet, D; Levy, Daniel; Goodrich, Cecilie A.; Campbell, Scott S.; Gillin, J. Christian

doi:10.1016/0893-133x(88)90004-8

Cited by 88 publications

(33 citation statements)

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“…Globally, H mice had fragmented sleep, with notably a shorter duration of SWS bouts and a greater number of wake episodes, higher amounts of SWS 1 and REM sleep, and a shorter latency of this stage. These sleepwakefulness alterations in H mice are consistent with the data obtained in various depression models in the rat (Adrien et al, 1991;Dugovic et al, 2000;Nestler et al, 2002;Shiromani et al, 1988). Furthermore, they are reminiscent of sleep impairments observed in depressed patients, notably the sleep fragmentation, the shift towards lighter sleep stages, and the enhanced REM sleep pressure (Benca, 2000;Gillin et al, 1991).…”

Section: Locomotor Activity and Sleep-wakefulness Cycles Under Baselisupporting

confidence: 86%

“…Sleep patterns are under the regulatory influence of several neurotransmitter systems among which the cholinergic and serotoninergic ones are prominent, notably regarding REM sleep expression (Pace-Schott and Hobson, 2002;Shiromani et al, 1988). In particular, REM sleep is enhanced following treatments with cholinergic agonists in rats (Baghdoyan, 1997), mice (Coleman et al, 2004), and humans (Seifritz et al, 1998;Sitaram and Gillin, 1980).…”

Section: Muscarinic-and 5-ht 1a -Receptor-mediated Regulations Of Remmentioning

confidence: 99%

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Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

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In depressed patients, sleep undergoes marked alterations, especially sleep onset insomnia, sleep fragmentation, and disturbances of the Rapid Eye Movement (REM) sleep. Abnormalities of rest-activity rhythms and of hypothalamic-pituitary-adrenocortical function have also been described in these patients. In the present study, we examined the presence of such abnormalities in a recently developed line of mice (Helpless mice-H) that exhibit depression-like behaviors in validated tests, compared to the nonhelpless (NH) line derived from the same colony. Experiments were essentially carried out in females for which previous studies showed marked differences between H and NH lines. Compared to NH mice, the H line exhibited (i) lower basal locomotor activity, (ii) sleep fragmentation, shift towards lighter sleep stages, and facilitation of REM sleep reflected by increased amounts and decreased latency, (iii) larger response to the REM sleep promoting effect of muscarinic receptor stimulation (by arecoline). In contrast, H and NH mice were equally responsive to the REM sleep inhibitory effect of 5-HT 1A receptor stimulation (by 8-OH-DPAT). In addition, a deficiency in delta power enhancement after sleep deprivation was observed in the H group, and acute immobilization stress in this group failed to elicit a REM sleep rebound and was associated with a long-lasting raise in serum corticosterone levels. These results further validate H mice as a depression model and suggest they might be of particular interest for investigating the neurobiological mechanisms and possibly genetic substrates underlying sleep alterations associated with depression.

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Section: Locomotor Activity and Sleep-wakefulness Cycles Under Baselisupporting

confidence: 86%

Section: Muscarinic-and 5-ht 1a -Receptor-mediated Regulations Of Remmentioning

confidence: 99%

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Popa

Yacoubi²,

Vaugeois³

et al. 2005

Neuropsychopharmacol

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“…However, numerous previous PPT lesion studies in both cats (Shouse and Siegel 1992;Webster and Jones 1988) and rats (Deurveilher and Hennevin 2001) have shown that the elimination PPT cholinergic cells suppressed physiological REM sleep. Moreover, one study has shown that rats with inbred cholinergic hyperfunction have excess REM sleep (Shiromani et al 1988). More recently, it has also been shown that, in the animal model of Alzheimer's, impaired REM sleep is caused by the reduction of cholinergic cells in the PPT (Zhang et al 2005).…”

Section: Discussionmentioning

confidence: 99%

Activation of Pedunculopontine Tegmental PKA Prevents GABA_B Receptor Activation–Mediated Rapid Eye Movement Sleep Suppression in the Freely Moving Rat

Datta¹

2007

Journal of Neurophysiology

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Datta S. Activation of pedunculopontine tegmental PKA prevents GABA B receptor activation-mediated rapid eye movement sleep suppression in the freely moving rat. J Neurophysiol 97: 3841-3850, 2007. First published April 4, 2007 doi:10.1152/jn.00263.2007. The pedunculopontine tegmental (PPT) GABAergic system plays a crucial role in the regulation of rapid eye movement (REM) sleep. I recently reported that the activation of PPT GABA B receptors suppressed REM sleep by inhibiting REM-ON cells. One of the important mechanisms for GABA B receptor activation-mediated physiological action is the inhibition of the intracellular cAMP-dependent protein kinase A (cAMP-PKA) signaling pathway. Accordingly, I hypothesized that the PPT GABA B receptor activation-mediated REM sleep suppression effect could be mediated through inhibition of cAMP-PKA activation. To test this hypothesis, a GABA B receptor selective agonist, baclofen hydrochloride (baclofen), cAMP-PKA activator, Spadenosine 3Ј,5Ј-cyclic monophosphothioate triethylamine (SpCAMPS), and vehicle control were microinjected into the PPT in selected combinations to determine effects on sleep-waking states of chronically instrumented, freely moving rats. Microinjection of SpCAMPS (1.5 nmol) induced REM sleep within a short latency (12.1 Ϯ 3.6 min) compared with vehicle control microinjection (60.0 Ϯ 6.5 min). On the contrary, microinjection of baclofen (1.5 nmol) suppressed REM sleep by delaying its appearance for ϳ183 min; however, the suppression of REM sleep by baclofen was prevented by a subsequent microinjection of SpCAMPS. These results provide evidence that the activation of cAMP-PKA within the PPT can successfully block the GABA B receptor activation-mediated REM sleep suppression effect. These findings suggest that the PPT GABA B receptor activationmediated REM sleep regulating mechanism involves inactivation of cAMP-PKA signaling in the freely moving rat.

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“…132 Since the Flinders Sensitive rat line also show increased responses to an anti-cholinergic agent, some animal models of depression with elevated REM sleep may resemble depressed human patients in terms of hypercholinergic reactivity. 122,[133][134][135] Again, these observations emphasize that elevated REM sleep is a credible marker for the animal models of depression.…”

mentioning

confidence: 95%

Sleep electroencephalography as a biomarker in depression

Steiger¹,

Pawlowski²,

Kimura³

2015

CPT

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Abstract:The sleep electroencephalogram (EEG) provides biomarkers of depression, which may help with diagnosis, prediction of therapy response, and prognosis in the treatment of depression. In patients with depression, characteristic sleep EEG changes include impaired sleep continuity, disinhibition of rapid-eye-movement (REM) sleep, and impaired non-REM sleep. Most antidepressants suppress REM sleep in depressed patients, healthy volunteers, and in animal models. REM suppression appears to be an important, but not an absolute requirement, for antidepressive effects of a substance. Enhanced REM density, a measure for frequency of REM, characterizes high-risk probands for affective disorders. REM-sleep changes were also found in animal models of depression. Sleep-EEG variables were shown to predict the response to treatment with antidepressants. Furthermore, certain clusters of sleep EEG variables predicted the course of the disorder for several years. Some of the predicted sleep EEG markers appear to be related to hypothalamic-pituitary-adrenal system activity.

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Increased REM sleep in rats selectively bred for cholinergic hyperactivity

Cited by 88 publications

References 0 publications

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Activation of Pedunculopontine Tegmental PKA Prevents GABA_B Receptor Activation–Mediated Rapid Eye Movement Sleep Suppression in the Freely Moving Rat

Sleep electroencephalography as a biomarker in depression

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Increased REM sleep in rats selectively bred for cholinergic hyperactivity

Cited by 88 publications

References 0 publications

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Homeostatic Regulation of Sleep in a Genetic Model of Depression in the Mouse: Effects of Muscarinic and 5-HT1A Receptor Activation

Activation of Pedunculopontine Tegmental PKA Prevents GABAB Receptor Activation–Mediated Rapid Eye Movement Sleep Suppression in the Freely Moving Rat

Sleep electroencephalography as a biomarker in depression

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Activation of Pedunculopontine Tegmental PKA Prevents GABA_B Receptor Activation–Mediated Rapid Eye Movement Sleep Suppression in the Freely Moving Rat