Sleep Recovery Improves Cognitive Function and Reduces Oxidative Stress and Beta-Amyloid Expression in the Hippocampus of Total Sleep-Deprived Adult Male Wistar Rats
Yıl 2026,
Cilt: 13 Sayı: 1
,
8
-
17
,
31.03.2026
Ubong Ekpo
,
Uduak Umana
,
Abubakar Sadeeq
,
Sohnap Sambo
Öz
Background: Lack of sleep has been linked in studies to increased beta-amyloid levels, oxidative stress, and memory impairments. Furthermore, sleep is known to help clear toxins that accumulate in the brain. Aim: This study investigated the restorative potentials of recovery sleep on total sleep deprivation-induced memory impairment, oxidative stress and changes in beta amyloid plaques in the hippocampus of adult male Wistar rats. Materials and Methods: Twenty-four male Wistar rats weighing between 150 and 200 g were divided into four groups. Group I remained in their home cages, while Groups II, III, and IV underwent sleep deprivation for 5 days. Groups III and IV then had recovery periods of 7 and 21 days, respectively. Spatial learning and memory was measured using the Morris Water Maze test. The rats were euthanized with ketamine, oxidative stress was analyzed using hippocampal tissue homogenate and beta-amyloid plaques in the CA1 and CA3 regions using Congo red stain. Results: Comparing the sleep-deprived group to the sleep-recovered group, the discrimination ratio increased significantly (p < 0.0001). Sleep recovery also decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malonaldehyde (MDA) and corticosterone (p < 0.01). Additionally, extracellular amyloid-beta expression in the CA1 and CA3 regions of the sleep recovery groups was significantly reduced (p < 0.0001 and p < 0.01). Conclusion: Recovery sleep was found to improve memory and decrease beta amyloid expression and oxidative stress in the CA1 and CA3 areas of the hippocampus.
Etik Beyan
Ethical approval was obtained from the Ahmadu Bello University Ethics Committee on Animal Use and Care by the institution’s established policies and procedures, with permission number ABUCAUC/2024/034.
Destekleyen Kurum
Ahmadu Bello University, Zaria
Proje Numarası
ABUCAUC/2024/034
Teşekkür
The authors acknowledge the staff of the Histology and Neuroscience Units of the Department of Human Anatomy, Ahmadu Bello University, Zaria, for the huge supports towards the accomplishment of this work.
Kaynakça
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Sleep Recovery Improves Cognitive Function and Reduces Oxidative Stress and Beta-Amyloid Expression in the Hippocampus of Total Sleep-Deprived Adult Male Wistar Rats
Yıl 2026,
Cilt: 13 Sayı: 1
,
8
-
17
,
31.03.2026
Ubong Ekpo
,
Uduak Umana
,
Abubakar Sadeeq
,
Sohnap Sambo
Öz
Background: Lack of sleep has been linked in studies to increased beta-amyloid levels, oxidative stress, and memory impairments. Furthermore, sleep is known to help clear toxins that accumulate in the brain. Aim: This study investigated the restorative potentials of recovery sleep on total sleep deprivation-induced memory impairment, oxidative stress and changes in beta amyloid plaques in the hippocampus of adult male Wistar rats. Materials and Methods: Twenty-four male Wistar rats weighing between 150 and 200 g were divided into four groups. Group I remained in their home cages, while Groups II, III, and IV underwent sleep deprivation for 5 days. Groups III and IV then had recovery periods of 7 and 21 days, respectively. Spatial learning and memory was measured using the Morris Water Maze test. The rats were euthanized with ketamine, oxidative stress was analyzed using hippocampal tissue homogenate and beta-amyloid plaques in the CA1 and CA3 regions using Congo red stain. Results: Comparing the sleep-deprived group to the sleep-recovered group, the discrimination ratio increased significantly (p < 0.0001). Sleep recovery also decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malonaldehyde (MDA) and corticosterone (p < 0.01). Additionally, extracellular amyloid-beta expression in the CA1 and CA3 regions of the sleep recovery groups was significantly reduced (p < 0.0001 and p < 0.01). Conclusion: Recovery sleep was found to improve memory and decrease beta amyloid expression and oxidative stress in the CA1 and CA3 areas of the hippocampus.
Etik Beyan
Ethical approval was obtained from the Ahmadu Bello University Ethics Committee on Animal Use and Care by the institution’s established policies and procedures, with permission number ABUCAUC/2024/034.
Destekleyen Kurum
Ahmadu Bello University, Zaria
Proje Numarası
ABUCAUC/2024/034
Teşekkür
The authors acknowledge the staff of the Histology and Neuroscience Units of the Department of Human Anatomy, Ahmadu Bello University, Zaria, for the huge supports towards the accomplishment of this work.
Kaynakça
-
1. Medic G, Wille M, Hemels ME. Short- and long-term health consequences of sleep disruption. Nat Sci Sleep. 2017;9:151-161. doi: 10.2147/NSS.S134864 [1].
-
2. Kordestani-Moghadam P, Nasehi M, Vaseghi S, Khodagholi F, Zarrindast MR. The role of sleep disturbances in depressive-like behavior with emphasis on α-ketoglutarate dehydrogenase activity in rats. Physiol Behav. 2020;224:113023. doi: 10.1016/j.physbeh.2020.113023 [2].
-
3. Mahdavi MS, Nasehi M, Vaseghi S, Mousavi Z, Zarrindast MR. The effect of alpha lipoic acid on passive avoidance and social interaction memory, pain perception, and locomotor activity in REM sleep-deprived rats. Pharmacol Rep. 2021;73(1):102-110. doi: 10.1007/s43440-020-00161-8 [3].
-
4. Eydipour Z, Nasehi M, Vaseghi S, Jamaldini SH, Zarrindast MR. The role of 5-HT4 serotonin receptors in the CA1 hippocampal region on memory acquisition impairment induced by total (TSD) and REM sleep deprivation (RSD). Physiol Behav. 2020;215:112788. doi: 10.1016/j.physbeh.2019.112788 [4].
-
5. Javad-Moosavi BZ, Nasehi M, Vaseghi S, Jamaldini SH, Zarrindast MR. Activation and inactivation of nicotinic receptors in the dorsal hippocampal region restored negative effects of total (TSD) and REM sleep deprivation (RSD) on memory acquisition, locomotor activity and pain perception. Neuroscience. 2020;433:200-211. doi: 10.1016/j.neuroscience.2020.03.006 [5].
-
6. Zhang J, Zhang L, Chang Y, et al. The endocannabinoid system contributes to memory deficits induced by rapid-eye-movement sleep deprivation in adolescent mice. Neuroscience. 2020;433:174-183. doi: 10.1016/j.neuroscience.2020.03.016 [6].
-
7. Kreutzmann JC, Havekes R, Abel T, Meerlo P. Sleep deprivation and hippocampal vulnerability: changes in neuronal plasticity, neurogenesis and cognitive function. Neuroscience. 2015;309:173-190. doi: 10.1016/j.neuroscience.2015.04.053 [7].
-
8. Klinzing JG, Niethard N, Born J. Mechanisms of systems memory consolidation during sleep. Nat Neurosci. 2019;22(10):1598-1610. doi: 10.1038/s41593-019-0467-3 [8].
-
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