The Potential Role of Nicotine in the Treatment of Learning and Memory Impairment after REM Sleep Deprivation

Purpose. The aim of this study was to assess the effect of melatonin in the proliferation of neural progenitors, melatonin concentration, and antiapoptotic proteins in the hippocampus of adult mice exposed to 96 h REM sleep deprivation (REMSD) prophylactic administration of melatonin for 14 days.Material and Methods. Five groups of Balb/C mice were used: (1) control, (2) REMSD, (3) melatonin (10 mg/kg) plus REMSD, (4) melatonin and intraperitoneal luzindole (once a day at 5 mg/kg) plus REMSD, and (5) luzindole plus REMSD. To measure melatonin content in hippocampal tissue we used HPLC. Bcl-2 and Bcl-xL proteins were measured by Western Blot and neurogenesis was determined by injecting 5-bromo-2-deoxyuridine (BrdU) and BrdU/nestin expressing cells in the subgranular zone of the dentate gyrus were quantified by epifluorescence.Results. The melatonin-treated REMSD group showed an increased neural precursor in 44% with respect to the REMSD group and in 28% when contrasted with the control group (P<0.021). The melatonin-treated REMSD group also showed the highest expression of Bcl-2 and Bcl-xL as compared to the rest of the groups.Conclusion. The exogenous administration of melatonin restores the tissue levels of sleep-deprived group and appears to be an efficient neuroprotective agent against the deleterious effects of REMSD.

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THE EFFECTS OF GLUCAGON-LIKE PEPTIDE 1 RECEPTOR AGONIST (EXENATİDE) ON MEMORY IMPAIRMENT, and ANXIETY- and DEPRESSION-LIKE BEHAVIOR INDUCED BY REM SLEEP DEPRIVATION

Brain Research Bulletin ◽

10.1016/j.brainresbull.2021.06.011 ◽

2021 ◽

Author(s):

Incı Turan ◽

Hale Sayan Ozacmak ◽

V. Haktan Ozacmak ◽

Meryem Ergenc ◽

Taner Bayraktaroğlu

Keyword(s):

Sleep Deprivation ◽

Rem Sleep ◽

Memory Impairment ◽

Receptor Agonist ◽

Anxiety And Depression ◽

Rem Sleep Deprivation ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

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Critical role of CA1 muscarinic receptors on memory acquisition deficit induced by total (TSD) and REM sleep deprivation (RSD)

Progress in Neuro-Psychopharmacology and Biological Psychiatry ◽

10.1016/j.pnpbp.2017.05.024 ◽

2017 ◽

Vol 79 ◽

pp. 128-135 ◽

Cited By ~ 9

Author(s):

Bibi-Zahra Javad-Moosavi ◽

Gholamhassan Vaezi ◽

Mohammad Nasehi ◽

Seyed-Ali Haeri-Rouhani ◽

Mohammad-Reza Zarrindast

Keyword(s):

Sleep Deprivation ◽

Muscarinic Receptors ◽

Rem Sleep ◽

Critical Role ◽

Rem Sleep Deprivation ◽

Memory Acquisition

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REM sleep promotes experience-dependent dendritic spine elimination in the mouse cortex

Nature Communications ◽

10.1038/s41467-020-18592-5 ◽

2020 ◽

Vol 11 (1) ◽

Cited By ~ 2

Author(s):

Yanmei Zhou ◽

Cora Sau Wan Lai ◽

Yang Bai ◽

Wei Li ◽

Ruohe Zhao ◽

...

Keyword(s):

Sleep Deprivation ◽

Neuronal Activity ◽

Rem Sleep ◽

Dendritic Spine ◽

Monocular Deprivation ◽

Association Cortex ◽

Synapse Elimination ◽

Rem Sleep Deprivation ◽

Calcium Spikes

Abstract In many parts of the nervous system, experience-dependent refinement of neuronal circuits predominantly involves synapse elimination. The role of sleep in this process remains unknown. We investigated the role of sleep in experience-dependent dendritic spine elimination of layer 5 pyramidal neurons in the visual (V1) and frontal association cortex (FrA) of 1-month-old mice. We found that monocular deprivation (MD) or auditory-cued fear conditioning (FC) caused rapid spine elimination in V1 or FrA, respectively. MD- or FC-induced spine elimination was significantly reduced after total sleep or REM sleep deprivation. Total sleep or REM sleep deprivation also prevented MD- and FC-induced reduction of neuronal activity in response to visual or conditioned auditory stimuli. Furthermore, dendritic calcium spikes increased substantially during REM sleep, and the blockade of these calcium spikes prevented MD- and FC-induced spine elimination. These findings reveal an important role of REM sleep in experience-dependent synapse elimination and neuronal activity reduction.

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