Activation of acetylcholine receptors and 5-HT 2 receptors have additive effects in the suppression of neocortical high-voltage spindles in aged rats

Jäkälä, Pekka; Puoliväli, Jukka; Björklund, Markus; Koivisto, Esa; Riekkinen, Paavo

doi:10.1007/s002130050345

Cited by 3 publications

(1 citation statement)

References 55 publications

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“…Moreover, we cannot exclude that blocking cholinergic neurotransmission impaired skill consolidation processes, additionally by affecting mechanisms associated with non-REM sleep. Thus, although high cholinergic activity suppresses sleep spindles (Puolivali et al, 1998;Jäkälä et al, 1997), it is still possible that some minimum cholinergic activity is required for spindle activity effectively supporting skill consolidation.…”

Section: Discussionmentioning

confidence: 99%

Impaired Off-Line Consolidation of Motor Memories After Combined Blockade of Cholinergic Receptors During REM Sleep-Rich Sleep

Rasch

Gais

Born

2009

Neuropsychopharmacol

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Rapid eye movement (REM) sleep has been considered important for the consolidation of memories, particularly of procedural skills. REM sleep, in contrast to slow-wave sleep (SWS), is hallmarked by the high, wake-like activity of the neurotransmitter acetylcholine (ACh), which promotes certain synaptic plastic processes underlying the formation of memories. Here, we show in healthy young men that off-line consolidation of a motor skill during a period of late sleep with high amounts of REM sleep depends essentially on high cholinergic activity. After a 3-h sleep period during the early night to satisfy the need for SWS, subjects learned a procedural finger sequence tapping task and a declarative word-pair learning task. After learning, they received either placebo or a combination of the muscarinic receptor antagonist scopolamine (4 mg/kg bodyweight, intravenously) and the nicotinic receptor antagonist mecamylamine (5 mg, orally), and then slept for another 3 h, ie, the late nocturnal sleep period, which is dominated by REM sleep. Retrieval was tested the following evening. Combined cholinergic receptor blockade significantly impaired motor skill consolidation, whereas word-pair memory remained unaffected. Additional data show that the impairing effect of cholinergic receptor blockade is specific to sleepdependent consolidation of motor skill and does not occur during a wake-retention interval. Taken together, these results identify high cholinergic activity during late, REM sleep-rich sleep as an essential factor promoting sleep-dependent consolidation of motor skills.

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Section: Discussionmentioning

confidence: 99%

Impaired Off-Line Consolidation of Motor Memories After Combined Blockade of Cholinergic Receptors During REM Sleep-Rich Sleep

Rasch

Gais

Born

2009

Neuropsychopharmacol

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Nicotinic modulation of neuronal networks: from receptors to cognition

et al. 2005

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Very little is known about mechanisms of how nAChR activation leads to a modification of electrical oscillation frequencies in EEGs. The results of studies using pharmacological interventions and transgenic animals implicate some nAChR types in aspects of cognition, but neuronal mechanisms are only poorly understood. We are only beginning to understand how nAChR distribution in neuronal networks impacts network functioning. Unveiling receptor and neuronal mechanisms important for nicotinic modulation of cognition will be instrumental for treatments of human disorders in which cholinergic signaling have been implicated, such as schizophrenia, attention deficit/hyperactivity disorder, and addiction.

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Ketanserin, a 5-HT2 receptor antagonist, decreases nicotine self-administration in rats

Levin

Slade

Johnson

et al. 2008

European Journal of Pharmacology

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Nicotine intake constitutes a principal mechanism for tobacco addiction. In addition to primary effects on nicotinic acetylcholine receptors, nicotine has cascading effects, which may underlie its neurobehavioral actions. Nicotine induces serotonin (5-HT) release, which has not classically been thought to be involved in tobacco addiction. However, addiction can be characterized more as a disorder of compulsion than a disorder of enjoyment. 5-HT mechanisms play key roles in compulsive disorders. Nicotine-induced 5-HT release may be a key to tobacco addiction. Ketanserin, a 5-HT2a and 2c receptor antagonist, significantly attenuates nicotine effects on attention and memory. These studies were conducted to determine if ketanserin would reduce nicotine self-administration in rats. Male Sprague-Dawley rats (N=12) were given initial food pellet training and then 10 sessions of nicotine self-administration training (0.03 mg/kg/infusion, i.v.). Then the rats were administered ketanserin (1 or 2 mg/kg, s.c.) or the saline vehicle. Ketanserin (2 mg/kg) significantly decreased nicotine self-administration. This did not seem to be due to sedative or amnestic effects of ketanserin. In a second study, the effects of repeated administration of 2 mg/kg ketanserin (N=11) vs. saline injections (N=10) were examined. In the initial phase, the acute effectiveness of ketanserin in significantly reducing nicotine self-administration was replicated. The effect became attenuated during the following several sessions, but the significant effect became re-established during the final phases of this two-week study. 5-HT mechanisms play critical roles in the maintenance of nicotine self-administration. Better understanding of those roles may help lead to new 5-HT-based treatments for tobacco addiction.

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Activation of acetylcholine receptors and 5-HT 2 receptors have additive effects in the suppression of neocortical high-voltage spindles in aged rats

Cited by 3 publications

References 55 publications

Impaired Off-Line Consolidation of Motor Memories After Combined Blockade of Cholinergic Receptors During REM Sleep-Rich Sleep

Impaired Off-Line Consolidation of Motor Memories After Combined Blockade of Cholinergic Receptors During REM Sleep-Rich Sleep

Nicotinic modulation of neuronal networks: from receptors to cognition

Ketanserin, a 5-HT2 receptor antagonist, decreases nicotine self-administration in rats

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