The Experts below are selected from a list of 210 Experts worldwide ranked by ideXlab platform
Karem H Alzoubi - One of the best experts on this subject based on the ideXlab platform.
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arbutus andrachne l reverses sleep deprivation induced memory impairments in rats
Molecular Neurobiology, 2018Co-Authors: Karem H Alzoubi, Omar F Khabour, Bayan S Malkawi, Tamam Elelimat, Feras Q AlaliAbstract:Sleep deprivation (SD) is associated with cognitive deficits. It was found to affect the hippocampus region of the brain by impairing memory formation. This impairment is suggested to be caused by elevation in oxidative stress in the body, including the brain during SD. It was hypothesized that the methanolic extract of the fruits of Arbutus andrachne L. (Ericaceae) will prevent chronic SD-induced impairment of hippocampal memory via its antioxidative properties. The methanolic extract of the fruits of A. andrachne was evaluated for its beneficial properties to reverse SD-induced cognitive impairment in rats. Animals were sleep deprived for 8 weeks using a Multiple Platform model. The extract was administered i.p. at three doses (50, 200, and 500 mg/kg). Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze (RAWM). In addition, the hippocampus was dissected to analyze the following oxidative stress markers: glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, glutathione peroxidase (GPx), and catalase. Chronic SD impaired short- and long-term memories (P < 0.05). Treatment of animals with A. andrachne fruit extract at all doses prevented long-term memory impairment induced by SD while such treatment prevented short-term memory impairment only at 200 and 500 mg/kg dose levels. Moreover, A. andrachne fruit extract normalized the reduction in the hippocampus GSH/GSSG ratio and activity of GPx, and catalase (P < 0.05) induced by chronic sleep deprivation. Chronic sleep deprivation impaired both short- and long-term memory formation, while methanolic extract of A. andrachne fruits reversed this impairment, probably through normalizing oxidative stress in the hippocampus.
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tempol prevents chronic sleep deprivation induced memory impairment
Brain Research Bulletin, 2016Co-Authors: Karem H Alzoubi, Omar F Khabour, Amal S Albawaana, Farah H Alhashimi, Rabaa Y AthamnehAbstract:Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using Multiple Platform model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.
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the combined effect of sleep deprivation and western diet on spatial learning and memory role of bdnf and oxidative stress
Journal of Molecular Neuroscience, 2013Co-Authors: Karem H Alzoubi, Omar F Khabour, Heba Salah, Baraa Abu E RashidAbstract:Either sleep deprivation or Western diet can impair learning and memory via induction of oxidative stress, which results in neuronal damage and interference with the neurotransmission. In this study, we examined the combined effect of sleep deprivation and Western diet on hippocampus-dependent spatial learning and memory. In addition, possible molecular targets for sleep deprivation and Western diet-induced cognitive impairments were investigated. Sleep deprivation was induced in rats using the modified Multiple Platform model simultaneous with the administration of Western diet for 6 weeks. Thereafter, spatial learning and memory were tested using radial arm water maze. At the molecular level, BDNF protein and antioxidant markers including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, and thiobarbituric acid reactive substances (TBARS) were assessed. The results of this study revealed that sleep deprivation, Western diet, or a combination of both impair short- and long-term memory (P < 0.05). The magnitude of the impairment induced by the combined treatment at the 24-h long-term memory was higher than that caused by each factor alone (P < 0.05). In addition, the combined treatment reduced the levels of hippocampal BDNF, a reduction that was not detected with each factor alone. Moreover, the combined treatment reduced the hippocampal activities of SOD, catalase, GPx, ratio of GSH/GSSG, and elevated TBARS level (P < 0.05). In conclusion, the combination of sleep deprivation and Western diet decreases BDNF levels and increases oxidative stress in the hippocampus, thus inducing memory impairment that is greater than the impairment produced by each factor alone.
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the neuroprotective effect of vitamin e on chronic sleep deprivation induced memory impairment the role of oxidative stress
Behavioural Brain Research, 2012Co-Authors: Karem H Alzoubi, Omar F Khabour, Baraa Abu E Rashid, Imad M Damaj, Heba SalahAbstract:Abstract Sleep deprivation induces oxidative stress and impairs learning and memory processes. Vitamin E, on the other hand, is a strong antioxidant that has neuroprotective effect on the brain. In this study, we examined the potential protective effect of chronic administration of vitamin E on chronic sleep deprivation-induced cognitive impairment. In addition, possible molecular targets for vitamin E effects on chronic sleep deprivation-induced cognitive impairment were determined. Sleep deprivation was induced in rats using modified Multiple Platform model. Vitamin E (100 mg/kg) was administered to animals by oral gavage. Behavioral study was conducted to test the spatial learning and memory using the radial arm water maze (RAWM). In addition, the hippocampus was dissected out and antioxidant markers including glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) were assessed. The results of this project revealed that chronic sleep deprivation impaired both (short- and long-term) memories (P
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post learning rem sleep deprivation impairs long term memory reversal by acute nicotine treatment
Neuroscience Letters, 2011Co-Authors: Abdulaziz M Aleisa, Karem H Alzoubi, Karim A AlkadhiAbstract:Rapid eye movement sleep deprivation (REM-SD) is associated with spatial learning and memory impairment. During REM-SD, an increase in nicotine consumption among habitual smokers and initiation of tobacco use by non-smokers have been reported. We have shown recently that nicotine treatment prevented learning and memory impairments associated with REM-SD. We now report the interactive effects of post-learning REM-SD and/or nicotine. The animals were first trained on the radial arm water maze (RAWM) task, then they were REM-sleep deprived using the modified Multiple Platform paradigm for 24h. During REM-SD period, the rats were injected with saline or nicotine (1mg/kg s.c. every 12h: a total of 3 injections). The animals were tested for long-term memory in the RAWM at the end of the REM-SD period. The 24h post-learning REM-SD significantly impaired long-term memory. However, nicotine treatment reversed the post-learning REM-SD-induced impairment of long-term memory. On the other hand, post-learning treatment of normal rats with nicotine for 24h enhanced long-term memory. These results indicate that post-learning acute nicotine treatment prevented the deleterious effect of REM-SD on cognitive abilities.
Sergio Tufik - One of the best experts on this subject based on the ideXlab platform.
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effects of sleep deprivation on maternal behaviour in animal models a systematic review and meta analysis
Journal of Sleep Research, 2021Co-Authors: Gabriel Natan Pires, Sergio Tufik, Thaina Baenninger De Oliveira, Victoria Feiner Ferreira De Mello, Andreia Gomes Bezerra, Cathalijn H C Leenaars, Merel Ritskeshoitinga, Monica L AndersenAbstract:Pregnancy is a period of numerous physical and emotional changes in women's lives, including alterations in sleep patterns and worsening of pre-existing sleep disturbances, which possibly lead to impaired postpartum maternal behaviour and mother-infant relationship. The effects of sleep deprivation during pregnancy in maternal behaviour have been evaluated in preclinical studies, but have provided inconsistent results. Thus, in the present study, we aimed to evaluate the effects of sleep deprivation during pregnancy on maternal behaviour of animals through a systematic review and meta-analyses. After a two-step selection process, six articles were included, all of them describing rat studies. The most frequently used method of sleep deprivation was rapid eye movement sleep restriction, using the Multiple-Platform method. Four meta-analyses were performed, none of them presenting significant impact of sleep deprivation on maternal behaviour, failing to reproduce the results observed in previous clinical studies. In conclusion, our results show a lack of translational applicability of animal models to evaluate the effects of sleep deprivation during pregnancy on maternal behaviour.
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sleep deprivation decreases the reproductive capacity by affecting the arrival of morulas in the uterus
Genesis, 2020Co-Authors: Bruno Frederico Aguilar Calegare, Sergio Tufik, Augusto Azzolini, Julia Ribeiro Da Silva Vallim, Edson Guimaraes Lo Turco, Priscila Farias Tempaku, Vanessa Cavalcante Da Silva, Vânia DalmeidaAbstract:A previous animal study by our group found that sleep deprivation during preimplantation was associated with decreased pregnancy maintenance. Given its impact on human society, we aimed in the current study to assess whether sleep deprivation affects blastocyst gene expression and/or the implantation process. For this, pregnant mice (gestational day 0 [GD 0]) were assigned into paradoxical sleep deprivation (SD, 72 hr; Multiple Platform method) and, a control (CT) group. Animals were euthanized on GD 3.5 and blood, uterus (embryos) and fallopian tube were collected. Then, 89% of CT presented blastocysts in the uterus versus 25% from SD group. Compared to CT, SD presented lighter relative uterus weight, increased plasma concentrations of corticosterone and testosterone, decreased concentrations of progesterone and luteinizing hormone, but no statistical differences in plasma concentrations of 17β-estradiol and follicle stimulating hormone. There were no differences in uterus and blastocyst gene expression related to embryo implantation and development, and no alteration in blastocysts global DNA methylation. Considering this, the decreased pregnancy maintenance after sleep deprivation seems not to be associated with implantation losses or developmental problems related to the blastocysts. It is likely that complications in morula development and/or its movement through the fallopian tubes affect the pregnancy rate, since only 25% of SD females presented a blastocyst on the GD 3.5. In fact, three out of four females without blastocysts in the uterus presented morula in the fallopian tubes due to a phase delay. Additionally, we suggest that the observed hormonal changes may play a role in this outcome.
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effects of acute and chronic sleep loss on immune modulation of rats
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2007Co-Authors: Adriano Zager, Monica L Andersen, Francieli Silva Ruiz, Isabela B Antunes, Sergio TufikAbstract:Sleep deprivation is now recognized as an increasingly common condition inherent to modern society, and one that in many ways, is detrimental to certain physiological systems, namely, immune function. Although sleep is now viewed by a significant body of researchers as being essential for the proper working of a host of defense systems, the consequences of a lack of sleep on immune function remains to be fully comprehended. The aim of the current study was to investigate how paradoxical sleep deprivation (PSD) for 24 and 96 h and sleep restriction (SR) for 21 days by the modified Multiple-Platform method, and their respective 24-h recovery periods, affect immune activation in rats. To this end, we assessed circulating white blood cell counts, lymphocyte count within immune organs, as well as Ig and complement production. The data revealed that PSD for 96 h increased complement C3 and corticosterone concentration in relation to the control group. In contrast, the spleen weight, total leukocytes, and lymphocytes decreased during SR for 21 days when compared with the control group, although production of a certain class of immunoglobulin, the IgM, did increase. After recovery sleep, lymphocyte count in axillary lymph nodes grew when rats had rebound sleep after PSD for 24 h, neutrophils increased after PSD 96 h and lymphocytes numbers were higher after SR 21 days. Such alterations during sleep deprivation suggest only minor alterations of nonspecific immune parameters during acute PSD, and a significant impairment in cellular response during chronic SR.
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effects of 3 nitropropionic acid administration on memory and hippocampal lipid peroxidation in sleep deprived mice
Progress in Neuro-psychopharmacology & Biological Psychiatry, 2007Co-Authors: Regina H Silva, Sergio Tufik, Vanessa C Abilio, Sonia R Kameda, Andre L Takatsucoleman, Rita C Carvalho, Rosana De A Ribeiro, Roberto FrussafilhoAbstract:Abstract Numerous studies have described memory deficits following sleep deprivation. There is also evidence that the absence of sleep increases brain oxidative stress. The present study investigates the effects of a pro-oxidant agent–3-nitropropionic acid (3-NP)–on hippocampal oxidative stress and passive avoidance performance of sleep-deprived mice. Mice were repeatedly treated i.p. with saline or 5 or 15 mg/kg 3-NP and sleep-deprived for 24 h by the Multiple Platform method—groups of 4–5 animals placed in water tanks, containing 12 Platforms (3 cm in diameter) surrounded by water up to 1 cm beneath the surface or kept in their home cage (control groups). The results showed that: (1) neither a 24 h sleep deprivation period nor 3-NP repeated treatment alone were able to induce memory deficits and increased hippocampal lipid peroxidation; (2) this same protocol of sleep deprivation, combined with 15 mg/kg 3-NP repeated treatment, induced memory deficits and an increase in hippocampal lipid peroxidation. The results support the involvement of hippocampal oxidative stress in the memory deficits induced by sleep deprivation and the hypothesis that normal sleep would prevent oxidative stress.
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effects of sleep deprivation on the development of autoimmune disease in an experimental model of systemic lupus erythematosus
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2006Co-Authors: Beatriz Duarte Palma, Alexandre Gabriel, Fernando Antonio Basile Colugnati, Sergio TufikAbstract:Sleep is hypothesized to play a restorative role on immune system. In addition, disturbed sleep is thought to impair host defense mechanisms. Chronic sleep deprivation is a common occurrence in modern society and has been observed in a number of chronic inflammatory conditions, such as systemic lupus erythematosus (SLE). New Zealand Black/New Zealand White (NZB/NZW) F1 mice develop an autoimmune disease that strongly resembles SLE in humans, exhibiting high titers of antinuclear antibodies associated with the development of rapidly progressive and lethal glomerulonephritis. On the basis of this evidence, the present study examined the onset and progress of lupus in as-yet healthy female mice submitted to sleep deprivation. Sleep deprivation was accomplished by two 96-h periods in the Multiple-Platform method when mice were 10 wk old, and they were observed until 28 wk of age. Blood samples were collected from the orbital plexus fortnightly to evaluate serum antinuclear antibodies and anti-double-stranded DNA. Proteinuria and longevity as well as body weight were also assessed. The results indicated that mice submitted to sleep deprivation exhibited an earlier onset of the disease, as reflected by the increased number of antinuclear antibodies. However, no statistical difference was found in the other parameters analyzed. According to these results, sleep deprivation could be considered as a risk factor for the onset but not for the evolution of the disease.
Donald E Campbell - One of the best experts on this subject based on the ideXlab platform.
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multisite comparison of cd4 and cd8 t lymphocyte counting by single versus Multiple Platform methodologies evaluation of beckman coulter flow count fluorospheres and the tetraone system
Clinical and Vaccine Immunology, 2000Co-Authors: Keith A Reimann, Maurice R G Ogorman, John Spritzler, Cynthia L Wilkening, Daniel E Sabath, Karen Helm, Donald E CampbellAbstract:The progressive loss of CD4+ T lymphocytes (CD4 T cells) through virally mediated cell destruction is the predominant pathophysiological manifestation of human immunodeficiency virus type 1 (HIV-1) infection (15). Enumeration of this cell subset provides an estimate of HIV disease progression (17). A major component of the immune response to HIV-1 infection is mediated by CD8+ T lymphocytes (CD8 T cells) (6). CD8 T cells capable of suppressing HIV-1 replication adopt an activation phenotype and appear in increased numbers in the blood and other body compartments following infection (7, 19). Therefore, the CD4 and CD8 T cells in blood are frequently quantified to assess immune competence and disease stage in HIV-1-infected patients. Furthermore, changes in CD4 T-cell numbers are an important estimate of the response to antiretroviral therapy. The CD4 T-cell count remains the most important immunologic surrogate marker of the efficacy of new antiretroviral regimens used in clinical trial evaluations (9). The accurate quantitation of these cells in blood is crucial for providing clinical care to HIV-1-infected patients and for the systematic evaluation of new therapeutic modalities. However, previous studies have identified substantial variability in results between laboratories performing these assays (1, 5). The currently recommended method for CD4 T-cell determination (2, 3) utilizes three independently derived values from two different instruments: a white blood cell (WBC) count and percent lymphocytes derived from a hematology instrument, and percentage of CD4 or CD8 T cells derived from a flow cytometer. A major disadvantage of this Multiple-Platform assay method is that error in each independent measurement is multiplied at each subsequent step in the calculation. Recently, new analytic methods have emerged that permit absolute CD4 and CD8 T-cell determinations to be performed either using a single-determination, non-flow cytometry-based assay (8, 10, 11) or entirely on the flow cytometer (14). In the single-Platform flow cytometry-based techniques, fluorospheres are added to the blood at a known concentration. Absolute cell counts in each specimen can be calculated ratiometrically by simultaneously counting both fluorospheres and the cells of interest (18). Other technological improvements, including automated instrument setup, lymphocyte gating, and cursor placement, could also improve assay performance. In the present study, we have assessed the within-laboratory and between-laboratory precision of two alternative assay methods: a two-color method that uses Beckman Coulter Flow-Count fluorospheres to determine absolute counts, and a four-color method that uses the fully automated tetraONE System. The precision obtained with these alternative methods was compared with the precision obtained with a conventional Multiple-Platform assay method. We also assessed the accuracy of these two new assay methods by comparing the absolute counts obtained with the single-Platform methods and with the conventional Multiple-Platform method.
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multisite comparison of cd4 and cd8 t lymphocyte counting by single versus Multiple Platform methodologies evaluation of beckman coulter flow count fluorospheres and the tetraone system the niaid daids new technologies evaluation group
Clinical and Vaccine Immunology, 2000Co-Authors: Keith A Reimann, Maurice R G Ogorman, John Spritzler, Cynthia L Wilkening, Daniel E Sabath, Karen Helm, Donald E CampbellAbstract:New analytic methods that permit absolute CD4 and CD8 T-cell determinations to be performed entirely on the flow cytometer have the potential for improving assay precision and accuracy. In a multisite trial, we compared two different single-Platform assay methods with a predicate two-color assay in which the absolute lymphocyte count was derived by conventional hematology. A two-color method employing lymphocyte light scatter gating and Beckman Coulter Flow-Count fluorospheres for absolute counting produced within-laboratory precision equivalent to that of the two-color predicate method, as measured by coefficient of variation of replicate measurements. The fully automated Beckman Coulter tetraONE System four-color assay employing CD45 lymphocyte gating, automated analysis, and absolute counting by fluorospheres resulted in a small but significant improvement in the within-laboratory precision of CD4 and CD8 cell counts and percentages suggesting that the CD45 lymphocyte gating and automated analysis might have contributed to the improved performance. Both the two-color method employing Flow-Count fluorospheres and the four-color tetraONE System provided significant and substantial improvements in between-laboratory precision of absolute counts. In some laboratories, absolute counts obtained by the single-Platform methods showed small but consistent differences relative to the predicate method. Comparison of each laboratory's absolute counts with the five-laboratory median value suggested that these differences resulted from a bias in the absolute lymphocyte count obtained from the hematology instrument in some laboratories. These results demonstrate the potential for single-Platform assay methods to improve within-laboratory and between-laboratory precision of CD4 and CD8 T-cell determinations compared with conventional assay methods.
Karim A Alkadhi - One of the best experts on this subject based on the ideXlab platform.
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the beneficial effects of regular exercise on cognition in rem sleep deprivation behavioral electrophysiological and molecular evidence
Neurobiology of Disease, 2012Co-Authors: Munder Zagaar, Ibrahim A Alhaider, An T Dao, Amber T Levine, Ahmed Alkarawi, Mariam Alzubaidy, Karim A AlkadhiAbstract:Inadequate sleep is prevalent in modern societies and is known to profoundly impair cognitive function. We examined the impact of 4 weeks of regular treadmill exercise on sleep deprivation induced spatial learning and memory, synaptic plasticity and related signaling molecules in area CA1 of the rat hippocampus. Rats were exercised on a treadmill and subsequently sleep-deprived for 24h using the modified Multiple Platform technique. Testing of learning and short-term memory performance in the radial arm water maze showed that although sedentary sleep deprived rats were severely impaired, exercised sleep deprived rats' performance was normal. Extracellular recording from area CA1 of anesthetized rats revealed that early phase LTP (E-LTP) was markedly impaired in the sedentary sleep deprived animals, but was normal in the exercised sleep deprived group. Additionally, immunoblot analysis of CA1 area before (basal) and after expression of E-LTP indicated that the significant down-regulation of the brain derived neurotrophic factor (BDNF) and phosphorylated calcium-calmodulin dependent protein kinase II (P-CaMKII) levels in sleep deprived animals was prevented by the regular exercise regimen. The results suggest that the regular exercise protocol prevents the sleep deprivation induced impairments in short-term memory and E-LTP by preventing deleterious changes in the basal and post-stimulation levels of P-CaMKII and BDNF associated with sleep deprivation.
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post learning rem sleep deprivation impairs long term memory reversal by acute nicotine treatment
Neuroscience Letters, 2011Co-Authors: Abdulaziz M Aleisa, Karem H Alzoubi, Karim A AlkadhiAbstract:Rapid eye movement sleep deprivation (REM-SD) is associated with spatial learning and memory impairment. During REM-SD, an increase in nicotine consumption among habitual smokers and initiation of tobacco use by non-smokers have been reported. We have shown recently that nicotine treatment prevented learning and memory impairments associated with REM-SD. We now report the interactive effects of post-learning REM-SD and/or nicotine. The animals were first trained on the radial arm water maze (RAWM) task, then they were REM-sleep deprived using the modified Multiple Platform paradigm for 24h. During REM-SD period, the rats were injected with saline or nicotine (1mg/kg s.c. every 12h: a total of 3 injections). The animals were tested for long-term memory in the RAWM at the end of the REM-SD period. The 24h post-learning REM-SD significantly impaired long-term memory. However, nicotine treatment reversed the post-learning REM-SD-induced impairment of long-term memory. On the other hand, post-learning treatment of normal rats with nicotine for 24h enhanced long-term memory. These results indicate that post-learning acute nicotine treatment prevented the deleterious effect of REM-SD on cognitive abilities.
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acute nicotine treatment prevents rem sleep deprivation induced learning and memory impairment in rat
Hippocampus, 2010Co-Authors: Abdulaziz M Aleisa, Karem H Alzoubi, Ibrahim A Alhaider, Gouda K Helal, Marisa Srivareerat, Trinh T Tran, Salim S Alrejaie, Karim A AlkadhiAbstract:Rapid eye movement (REM) sleep deprivation (SD) is implicated in impairment of spatial learning and memory and hippocampal long-term potentiation (LTP). An increase in nicotine consumption among habitual smokers and initiation of tobacco use by nonsmokers was observed during SD. Although nicotine treatment was reported to attenuate the impairment of learning and memory and LTP associated with several mental disorders, the effect of nicotine on SD-induced learning and memory impairment has not been studied. Modified Multiple Platform paradigm was used to induce SD for 24 or 48 h during which rats were injected with saline or nicotine (1 mg kg(-1) s.c.) twice a day. In the radial arm water maze (RAWM) task, 24- or 48-h SD significantly impaired learning and short-term memory. In addition, extracellular recordings from CA1 and dentate gyrus (DG) regions of the hippocampus in urethane anesthetized rats showed a significant impairment of LTP after 24- and 48-h SD. Treatment of normal rats with nicotine for 24 or 48 h did not enhance spatial learning and memory or affect magnitude of LTP in the CA1 and DG regions. However, concurrent, acute treatment of rats with nicotine significantly attenuated SD-induced impairment of learning and STM and prevented SD-induced impairment of LTP in the CA1 and DG regions. These results show that acute nicotine treatment prevented the deleterious effect of sleep loss on cognitive abilities and synaptic plasticity.
Omar F Khabour - One of the best experts on this subject based on the ideXlab platform.
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arbutus andrachne l reverses sleep deprivation induced memory impairments in rats
Molecular Neurobiology, 2018Co-Authors: Karem H Alzoubi, Omar F Khabour, Bayan S Malkawi, Tamam Elelimat, Feras Q AlaliAbstract:Sleep deprivation (SD) is associated with cognitive deficits. It was found to affect the hippocampus region of the brain by impairing memory formation. This impairment is suggested to be caused by elevation in oxidative stress in the body, including the brain during SD. It was hypothesized that the methanolic extract of the fruits of Arbutus andrachne L. (Ericaceae) will prevent chronic SD-induced impairment of hippocampal memory via its antioxidative properties. The methanolic extract of the fruits of A. andrachne was evaluated for its beneficial properties to reverse SD-induced cognitive impairment in rats. Animals were sleep deprived for 8 weeks using a Multiple Platform model. The extract was administered i.p. at three doses (50, 200, and 500 mg/kg). Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze (RAWM). In addition, the hippocampus was dissected to analyze the following oxidative stress markers: glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, glutathione peroxidase (GPx), and catalase. Chronic SD impaired short- and long-term memories (P < 0.05). Treatment of animals with A. andrachne fruit extract at all doses prevented long-term memory impairment induced by SD while such treatment prevented short-term memory impairment only at 200 and 500 mg/kg dose levels. Moreover, A. andrachne fruit extract normalized the reduction in the hippocampus GSH/GSSG ratio and activity of GPx, and catalase (P < 0.05) induced by chronic sleep deprivation. Chronic sleep deprivation impaired both short- and long-term memory formation, while methanolic extract of A. andrachne fruits reversed this impairment, probably through normalizing oxidative stress in the hippocampus.
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tempol prevents chronic sleep deprivation induced memory impairment
Brain Research Bulletin, 2016Co-Authors: Karem H Alzoubi, Omar F Khabour, Amal S Albawaana, Farah H Alhashimi, Rabaa Y AthamnehAbstract:Sleep deprivation is associated with oxidative stress that causes learning and memory impairment. Tempol is a nitroxide compound that promotes the metabolism of many reactive oxygen species (ROS) and has antioxidant and neuroprotective effect. The current study investigated whether chronic administration of tempol can overcome oxidative stress and prevent learning and memory impairment induced by sleep deprivation. Sleep deprivation was induced in rats using Multiple Platform model. Tempol was administered to rats via oral gavages. Behavioral studies were conducted to test the spatial learning and memory using radial arm water maze. The hippocampus was dissected; antioxidant biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) were assessed. The result of this project revealed that chronic sleep deprivation impaired both short and long term memory (P<0.05), while tempol treatment prevented such effect. Furthermore, tempol normalized chronic sleep deprivation induced reduction in the hippocampus activity of catalase, GPx, and SOD (P<0.05). Tempol also enhanced the ratio of GSH/GSSG in chronically sleep deprived rats treated with tempol as compared with only sleep deprived rats (P<0.05). In conclusion chronic sleep deprivation induced memory impairment, and treatment with tempol prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.
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the combined effect of sleep deprivation and western diet on spatial learning and memory role of bdnf and oxidative stress
Journal of Molecular Neuroscience, 2013Co-Authors: Karem H Alzoubi, Omar F Khabour, Heba Salah, Baraa Abu E RashidAbstract:Either sleep deprivation or Western diet can impair learning and memory via induction of oxidative stress, which results in neuronal damage and interference with the neurotransmission. In this study, we examined the combined effect of sleep deprivation and Western diet on hippocampus-dependent spatial learning and memory. In addition, possible molecular targets for sleep deprivation and Western diet-induced cognitive impairments were investigated. Sleep deprivation was induced in rats using the modified Multiple Platform model simultaneous with the administration of Western diet for 6 weeks. Thereafter, spatial learning and memory were tested using radial arm water maze. At the molecular level, BDNF protein and antioxidant markers including superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG, and thiobarbituric acid reactive substances (TBARS) were assessed. The results of this study revealed that sleep deprivation, Western diet, or a combination of both impair short- and long-term memory (P < 0.05). The magnitude of the impairment induced by the combined treatment at the 24-h long-term memory was higher than that caused by each factor alone (P < 0.05). In addition, the combined treatment reduced the levels of hippocampal BDNF, a reduction that was not detected with each factor alone. Moreover, the combined treatment reduced the hippocampal activities of SOD, catalase, GPx, ratio of GSH/GSSG, and elevated TBARS level (P < 0.05). In conclusion, the combination of sleep deprivation and Western diet decreases BDNF levels and increases oxidative stress in the hippocampus, thus inducing memory impairment that is greater than the impairment produced by each factor alone.
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the neuroprotective effect of vitamin e on chronic sleep deprivation induced memory impairment the role of oxidative stress
Behavioural Brain Research, 2012Co-Authors: Karem H Alzoubi, Omar F Khabour, Baraa Abu E Rashid, Imad M Damaj, Heba SalahAbstract:Abstract Sleep deprivation induces oxidative stress and impairs learning and memory processes. Vitamin E, on the other hand, is a strong antioxidant that has neuroprotective effect on the brain. In this study, we examined the potential protective effect of chronic administration of vitamin E on chronic sleep deprivation-induced cognitive impairment. In addition, possible molecular targets for vitamin E effects on chronic sleep deprivation-induced cognitive impairment were determined. Sleep deprivation was induced in rats using modified Multiple Platform model. Vitamin E (100 mg/kg) was administered to animals by oral gavage. Behavioral study was conducted to test the spatial learning and memory using the radial arm water maze (RAWM). In addition, the hippocampus was dissected out and antioxidant markers including glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG, glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD) were assessed. The results of this project revealed that chronic sleep deprivation impaired both (short- and long-term) memories (P
