The cholinergic REM sleep induction test with pilocarpine in mildly depressed patients and normal controls

Kenny, William M.; Sutton, Laura; Golshan, Shahrokh; Ruiz, Caroline; Kelsoe, John R.; Rapaport, Mark Hyman; Gillin, J. Christian

doi:10.1016/0006-3223(93)90275-i

Cited by 21 publications

(8 citation statements)

References 34 publications

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“…(23, 24) demonstrated a significantly stronger reduction of this interval in depressed patients compared with healthy subjects. These results were not replicated with pilocarpine (25).…”

Section: The Reciprocal Interaction Model Of Non‐rem and Rem Sleep Rementioning

confidence: 85%

Sleep and manipulations of the sleep–wake rhythm in depression

Berger

Calker

Riemann

2003

Acta Psychiatr Scand

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Objective: Disturbed sleep is typical for most depressed patients and complaints about disordered sleep are the hallmarks of the disorder. Polysomnographic sleep research has demonstrated that besides impaired sleep continuity, sleep in depression is characterized by a reduction of slow wave sleep and a disinhibition of random eye movement (REM) sleep, with a shortening of REM latency, a prolongation of the first REM period and increased REM density. Method: Our own experimental work has focused on the reciprocal interaction hypothesis of non‐REM and REM sleep regulation as a model to explain the characteristic features of depressed sleep. Results: In agreement with the major tenet of this model, administration of cholinomimetics provoked shortened REM latency in healthy subjects and led to an even stronger REM sleep disinhibition in depressed patients. Manipulations of the sleep–wake cycle, such as sleep deprivation or a phase advance of the sleep period, alleviate depressive symptoms. Conclusion: These data indicate a strong bidirectional relationship between sleep, sleep alterations and depression.

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“…(23, 24) demonstrated a significantly stronger reduction of this interval in depressed patients compared with healthy subjects. These results were not replicated with pilocarpine (25).…”

Section: The Reciprocal Interaction Model Of Non‐rem and Rem Sleep Rementioning

confidence: 85%

Sleep and manipulations of the sleep–wake rhythm in depression

Berger

Calker

Riemann

2003

Acta Psychiatr Scand

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“…In animals, early studies suggested a REM-promoting role for acetylcholine (410, 504) particularly when monoamines had been previously depleted by use of the agent reserpine (605). In humans, enhancement of cholinergic tone by systemic application of acetylcholinesterase inhibitors or muscarinic agonists (93, 513, 692, 1065, 1185, 1186) consistently decreases REM sleep latency and enhances REM sleep amount, particularly phasic REM events, whereas muscarinic antagonists cause the reverse effect (428, 625, 1051). Enhancement of monoaminergic tone with antidepressants is well known to result in a long-lasting suppression of REM in humans and animals.…”

Section: Rem Sleepmentioning

confidence: 99%

Control of Sleep and Wakefulness

Brown

Basheer

Mckenna

et al. 2012

Physiological Reviews

1,198

1,105

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This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.

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“…Post-sleep motor performance was reduced by oxotremorine, a muscarinic acetylcholine receptor agonist, suggesting that activation of muscarinic receptors is undesirable for memory consolidation during early sleep. We did not perform EEG recordings after oxotremorine injection but assume that it would have reduced NREM sleep while increasing REM sleep as reported in previous studies with other muscarinic ACh receptor agonists e.g., pilocarpine and RS-86 (Lauriello J et al 1993;Vanderwolf CH et al 1993;Dringenberg HC and CH Vanderwolf 1996;Nissen C et al 2006;Tejada S et al 2007) or knockout mice with deleted genes for muscarinic receptors Chrm1…”

Section: Discussionmentioning

confidence: 99%

Low acetylcholine during early sleep is important for motor memory consolidation

Qandeel

2018

Preprint

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The synaptic homeostasis theory of sleep proposes that low neurotransmitter activity in sleep is optimal for memory consolidation. We tested this theory by asking whether increasing acetylcholine levels during early sleep would disrupt motor memory consolidation. We trained separate groups of adult mice on the rotarod walking and skilled reaching for food tasks, and after training, administered physostigmine, an acetylcholinesterase inhibitor, to increase cholinergic tone in subsequent sleep. Post-sleep testing suggested that physostigmine impaired motor skill acquisition. Home-cage video monitoring and electrophysiology revealed that physostigmine disrupted sleep structure, delayed non-rapid-eyemovement sleep onset, and reduced slow-wave power in the hippocampus and cortex. The impaired motor performance with physostigmine, however, was not solely due to its effects on sleep structure, as one hour of sleep deprivation after training did not impair rotarod performance. A reduction in cholinergic tone by inactivation of cholinergic neurons during early sleep also affected rotarod performance. Administration of agonists and antagonists of muscarinic and nicotinic acetylcholine receptors revealed that activation of muscarinic receptors during early sleep impaired rotarod performance. The experiments suggest that the increased slow wave activity and inactivation of muscarinic receptors during early sleep due to reduced acetylcholine contribute to motor memory consolidation.

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The cholinergic REM sleep induction test with pilocarpine in mildly depressed patients and normal controls

Cited by 21 publications

References 34 publications

Sleep and manipulations of the sleep–wake rhythm in depression

Sleep and manipulations of the sleep–wake rhythm in depression

Control of Sleep and Wakefulness

Low acetylcholine during early sleep is important for motor memory consolidation

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