Learning deficits induced by sleep deprivation and recovery are not associated with altered [3H]muscimol and [3H]flunitrazepam binding

Dubiela, Francisco Paulino; Oliveira, Maria Gabriela Menezes; Moreira, Karin Di Monteiro; Nóbrega, José N.; Tufik, Sérgio; Hipólide, Débora Cristina

doi:10.1016/j.brainres.2005.01.005

Cited by 14 publications

(12 citation statements)

References 56 publications

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“…In fact, REMSD induced-increased locomotor activity in rats has been reported by some authors in rats (Suchecki et al, 2002; Tartar et al, 2009) and mice (Armani et al, 2012), but not by others (Dubiela et al, 2011); in the case of passive avoidance task, altered motor activity could be responsible for the short- (2 h post-training), but not for the long-term (24 h post-training) retention deficit (Dubiela et al, 2005), indicating, once again, that acquisition is impaired by REMSD.…”

Section: Introductionmentioning

confidence: 92%

“…Additional evidence of this relationship has been given by human and animal studies demonstrating that training in different memory tasks increases sleep time (Lucero, 1970; Smith et al, 1980; Smith and Lapp, 1986; Portell-Cortés et al, 1989; Smith and Rose, 1997) and that either sleep- (SD) or REM sleep deprivation (REMSD) before training impairs the performance of animals in numerous hippocampal-dependent tasks, such as inhibitory avoidance (Stern, 1971; Bueno et al, 1994, 2000; Gruart-Masso et al, 1995; Moreira et al, 2003; Dubiela et al, 2005), multiple trial inhibitory avoidance (Moreira et al, 2010; Ota et al, 2013), Morris water maze (Smith and Rose, 1996; Guan et al, 2004) and fear conditioning (Hicks et al, 1988; Dametto et al, 2002; McDermott et al, 2003; Tiba et al, 2008). However, results from studies using pre-training protracted REMSD protocols are difficult to interpret because the animals are under an altered sleep-waking pattern both before (sleep-deprived) and after training (when sleep rebound is taking place) thus, precluding conclusions as to whether this manipulation affects acquisition and/or consolidation of the information in these memory tasks.…”

Section: Introductionmentioning

confidence: 99%

“…Studies employing passive avoidance task show that 24 h of sleep recovery are sufficient to restore the performance of 96 h REM sleep-deprived rats (Dubiela et al, 2005, 2010), suggesting that SD-induced performance deficit may not be due to impairment of consolidation, but rather to some other unspecific effect, such as altered motor performance. In fact, REMSD induced-increased locomotor activity in rats has been reported by some authors in rats (Suchecki et al, 2002; Tartar et al, 2009) and mice (Armani et al, 2012), but not by others (Dubiela et al, 2011); in the case of passive avoidance task, altered motor activity could be responsible for the short- (2 h post-training), but not for the long-term (24 h post-training) retention deficit (Dubiela et al, 2005), indicating, once again, that acquisition is impaired by REMSD.…”

Section: Introductionmentioning

confidence: 99%

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Effects of sleep deprivation on different phases of memory in the rat: dissociation between contextual and tone fear conditioning tasks

Rossi¹,

Tiba²,

Moreira³

et al. 2014

Front. Behav. Neurosci.

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Numerous studies show that sleep deprivation (SD) impacts negatively on cognitive processes, including learning and memory. Memory formation encompasses distinct phases of which acquisition, consolidation and retrieval are better known. Previous studies with pre-training SD induced by the platform method have shown impairment in fear conditioning tasks. Nonetheless, pre-training manipulations do not allow the distinction between effects on acquisition and/or consolidation, interfering, ultimately, on recall of/performance in the task. In the present study, animals were first trained in contextual and tone fear conditioning (TFC) tasks and then submitted to SD with the purpose to evaluate the effect of this manipulation on different stages of the learning process, e.g., in the uptake of (new) information during learning, its encoding and stabilization, and the recall of stored memories. Besides, we also investigated the effect of SD in the extinction of fear memory and a possible state-dependent learning induced by this manipulation. For each task (contextual or TFC), animals were trained and then distributed into control, not sleep-deprived (CTL) and SD groups, the latter being submitted to the modified multiple platform paradigm for 96 h. Subsets of eight rats in each group/experiment were submitted to the test of the tasks, either immediately or at different time intervals after SD. The results indicated that (a) pre- but not post-training SD impaired recall in the contextual and TFC; (b) this impairment was not state-dependent; and (c) in the contextual fear conditioning (CFC), pre-test SD prevented extinction of the learned task. Overall, these results suggest that SD interferes with acquisition, recall and extinction, but not necessarily with consolidation of emotional memory.

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Section: Introductionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of sleep deprivation on different phases of memory in the rat: dissociation between contextual and tone fear conditioning tasks

Rossi¹,

Tiba²,

Moreira³

et al. 2014

Front. Behav. Neurosci.

Self Cite

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“…Firstly, systemic concomitant administration of ineffective doses of muscarinic and NMDAR antagonists produced amnesic effects in several tasks, such as spatial mazes [4], [5], contextual fear conditioning [1], inhibitory avoidance [6], [7] and a visual recognition memory task [8]. Recent studies confirmed significant deficits when sub-threshold doses were co-administered intracerebrally.…”

Section: Introductionmentioning

confidence: 99%

D-cycloserine in Prelimbic Cortex Reverses Scopolamine-Induced Deficits in Olfactory Memory in Rats

et al. 2013

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A significant interaction between N-methyl-D-aspartate (NMDA) and muscarinic receptors has been suggested in the modulation of learning and memory processes. The present study further investigates this issue and explores whether d-cycloserine (DCS), a partial agonist at the glycine binding site of the NMDA receptors that has been regarded as a cognitive enhancer, would reverse scopolamine (SCOP)-induced amnesia in two olfactory learning tasks when administered into the prelimbic cortex (PLC). Thus, in experiment 1, DCS (10 µg/site) was infused prior to acquisition of odor discrimination (ODT) and social transmission of food preference (STFP), which have been previously characterized as paradigms sensitive to PLC muscarinic blockade. Immediately after learning such tasks, SCOP was injected (20 µg/site) and the effects of both drugs (alone and combined) were tested in 24-h retention tests. To assess whether DCS effects may depend on the difficulty of the task, in the STFP the rats expressed their food preference either in a standard two-choice test (experiment 1) or a more challenging three-choice test (experiment 2). The results showed that bilateral intra-PLC infusions of SCOP markedly disrupted the ODT and STFP memory tests. Additionally, infusions of DCS alone into the PLC enhanced ODT but not STFP retention. However, the DCS treatment reversed SCOP-induced memory deficits in both tasks, and this effect seemed more apparent in ODT and 3-choice STFP. Such results support the interaction between the glutamatergic and the cholinergic systems in the PLC in such a way that positive modulation of the NMDA receptor/channel, through activation of the glycine binding site, may compensate dysfunction of muscarinic neurotransmission involved in stimulus-reward and relational learning tasks.

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“…injection with either vehicle or flunitrazepam and completion of the analysis of aggressive behavior, the rats were killed by decapitation and brains were rapidly removed, frozen over dry ice, and stored at −80°C. Binding assays for BZD sites were performed as described previously (Dubiela et al 2005), with minor modifications. Briefly, for histological processing, brains were first allowed to equilibrate to −18°C.…”

Section: Drugmentioning

confidence: 99%

Heightened aggression after chronic flunitrazepam in male rats: potential links to cortical and caudate–putamen-binding sites

et al. 2007

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Learning deficits induced by sleep deprivation and recovery are not associated with altered [3H]muscimol and [3H]flunitrazepam binding

Cited by 14 publications

References 56 publications

Effects of sleep deprivation on different phases of memory in the rat: dissociation between contextual and tone fear conditioning tasks

Effects of sleep deprivation on different phases of memory in the rat: dissociation between contextual and tone fear conditioning tasks

D-cycloserine in Prelimbic Cortex Reverses Scopolamine-Induced Deficits in Olfactory Memory in Rats

Heightened aggression after chronic flunitrazepam in male rats: potential links to cortical and caudate–putamen-binding sites

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