Role of central cholinergic receptor sub-types in spatial working memory: a five-arm maze task in mice provides evidence for a functional role of nicotinic receptors in mediating trace access processes

Maviel, Thibault; Durkin, Thomas

doi:10.1016/s0306-4522(03)00403-2

Cited by 18 publications

(6 citation statements)

References 64 publications

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“…Moreover, the separation of muscarinic and nicotinic contributions is hampered by interactions between the receptors. For example, selectively blocking the muscarinic receptors by scopolamine, through blocking M2 presynaptic autoreceptors, induces a pronounced increase in ACh release, which, in turn, can lead to an overactivation of post-synaptic nicotinic receptors (Maviel and Durkin, 2003;Durkin et al, 1992). Thus, modeling the effects of a generally lowered cholinergic neurotransmission requires that both the cholinergic receptor types are blocked simultaneously, thereby avoiding increased nicotinic activation.…”

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 receptor regulation is a complex process, as receptor up-regulation has been reported following desensitization, inactivation of receptor function, and loss of cholinergic input [1,16,20,26,48,59,63]. The present study was confined to the examination of changes in nicotinic binding in the PFC, as central nicotinic receptors have been shown to play a key role in the attentional processes enabling working memory trace access during retrieval, as well as in the modulation of synaptic plasticity [25,45]. However, it was not our goal to explore how changes in nACHr distribution within neural networks would affect cognitive function, clearly a valuable and worthy aim that is well beyond the scope of the present study.…”

Section: Discussionmentioning

confidence: 99%

Impaired spatial working memory and altered choline acetyltransferase (CHAT) immunoreactivity and nicotinic receptor binding in rats exposed to intermittent hypoxia during sleep

Row

Kheirandish

Cheng

et al. 2007

Behavioural Brain Research

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Exposure to intermittent hypoxia (IH), such as occurs in sleep-disordered breathing (SDB), is associated with cognitive impairment, neurodegeneration, oxidative stress, and inflammatory responses within rodent brain regions such as the basal forebrain. In this region, damage to cholinergic neurons correlates with working memory deficits in a number of neurodegenerative disorders, suggesting that degeneration of cholinergic systems may also contribute to the working memory impairments observed after IH exposures. We therefore examined basal forebrain choline acetyltransferase (CHAT) immunohistochemistry, nicotinic receptor binding in the prefrontal cortex (PFC), and working memory, in male rats tested on a delayed matching to place (DMP) task in the water maze following exposure to either room air (RA) or intermittent hypoxia (IH; alternating 90s epochs of 21% and 10% O(2) during sleep). IH-treated animals displayed impaired working memory with respect to controls, along with significant reductions in CHAT-stained neurons in the medial septal nucleus, in both the vertical and horizontal limbs of the diagonal band, and the substantia inominata after 14 days of IH exposure. In addition, increases in nicotinic binding and receptor affinity in the PFC were observed after 14 days of IH exposure. Thus, a loss of cholinergic neuronal phenotype in the basal forebrain may contribute to the cognitive impairments associated with CIH exposure. However, compensatory mechanisms may also be activated in other brain regions, and may provide potential therapeutic targets for the cognitive impairments associated with SDB.

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“…As spatial working memory is impaired by administration of anticholinergics (Kim and Levin 1996;Pilcher et al 1997), it may be that clozapine's greater antagonism at these muscarinic cholinergic receptors explains the lack of improvement. However, some authors have challenged the importance of muscarinic blockade in working memory deficits (Maviel and Durkin 2003). Alternatively, there may be differences in the way in which chronic treatment with clozapine and risperidone influences noradrenergic function.…”

Section: Discussionmentioning

confidence: 99%

Propranolol blocks chronic risperidone treatment-induced enhancement of spatial working memory performance of rats in a delayed matching-to-place water maze task

et al. 2007

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Role of central cholinergic receptor sub-types in spatial working memory: a five-arm maze task in mice provides evidence for a functional role of nicotinic receptors in mediating trace access processes

Cited by 18 publications

References 64 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

Impaired spatial working memory and altered choline acetyltransferase (CHAT) immunoreactivity and nicotinic receptor binding in rats exposed to intermittent hypoxia during sleep

Propranolol blocks chronic risperidone treatment-induced enhancement of spatial working memory performance of rats in a delayed matching-to-place water maze task

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