Nicotine reverses adult‐onset hypothyroidism‐induced impairment of learning and memory: Behavioral and electrophysiological studies

Alzoubi, Karem H.; Aleisa, Abdulaziz M.; Gerges, Nashaat Z.; Alkadhi, Karim A.

doi:10.1002/jnr.21014

Cited by 60 publications

(51 citation statements)

References 73 publications

(115 reference statements)

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“…While some show enhancement of ''normal'' memory as a result of nicotine treatment (Wesnes and Warburton, 1984;Levin et al, 1987Levin et al, , 1993Levin et al, , 1997Levin et al, , 2001Bancroft and Levin, 2000;Bettany and Levin, 2001;Swan and LessovSchlaggar, 2007; for review), others report no effect (Dunne et al, 1986;Parrott and Winder, 1989;Aleisa et al, 2006c;Alzoubi et al, 2006b), and even memory impairment (Sorenson et al, 1991;Park et al, 2000). In humans, however, the literature that describes nicotine effect on memory is sometimes confounded by the use of smokers as subjects (Swan and Lessov-Schlaggar, 2007;for review).…”

Section: Discussionmentioning

confidence: 92%

Acute nicotine treatment prevents rem sleep deprivation‐induced learning and memory impairment in rat

et al. 2011

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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.

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Section: Discussionmentioning

confidence: 92%

Acute nicotine treatment prevents rem sleep deprivation‐induced learning and memory impairment in rat

et al. 2011

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“…Previous studies have also shown that hypothyroidism disrupts learning and memory processes in neonatal and juvenile rats 18 . It has been documented that hypothyroidism attenuates hippocampal-related learning and memory, and long-term potentiation 19 . Reduced levels .…”

Section: Discussionmentioning

confidence: 99%

Thymoquinone reverses learning and memory impairments and brain tissue oxidative damage in hypothyroid juvenile rats

Baghcheghi

Hosseini

Beheshti

et al. 2018

Arq. Neuro-Psiquiatr.

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In this study, the effect of thymoquinone (TQ) on propylthiouracil (PTU)-induced memory impairment was investigated in juvenile rats. The rats were grouped into control, Hypo, Hypo-TQ5 and Hypo-TQ10. Propylthiouracil increased latency time in the Morris water maze test and decreased delay in entering the dark compartment in the passive avoidance test. Both 5 mg/kg and 10 mg/kg doses of TQ decreased latency time in the Morris water maze test and increased delay in entering the dark compartment in a passive avoidance test. The PTU also increased malondialdehyde and nitric oxide metabolites in the brain while reduced the thiol content and superoxide dismutase and catalase activities and serum T4 level. Both doses of TQ decreased malondialdehyde and nitric oxide metabolites in the brain while enhanced the thiol content and superoxide dismutase and catalase activities and serum T4 level. The results of the present study showed that TQ protected against PTU-induced memory impairments in rats.Keywords: hypothyroidism; propylthiouracil; memory RESUMO Neste estudo, foi investigado o efeito da timoquinona (TQ) contra deficiências de memória induzidas por propiltiouracilo (PTU) em ratos juvenis. Os ratos foram agrupados em grupos: controle, Hypo, Hypo-TQ5, e Hypo-TQ10. O PTU aumentou o tempo de latência no teste do labirinto aquático de Morris (MWM) e diminuiu o atraso para entrar no compartimento escuro no teste de evasão passiva (PA). Ambas as doses de TQ diminuíram o tempo de latência no teste de MWM e aumentaram o atraso para entrar no compartimento escuro no teste de PA. O PTU também aumentou os metabolitos de malondialdeído (MDA) e óxido nítrico (NO) no cérebro, enquanto reduziu o teor de tiol e as atividades de superóxido dismutasa (SOD) e catalasa (CAT) e o nível sérico de T4. Ambas as doses de TQ diminuíram os metabolitos de MDA e de NO no cérebro, aumentaram o conteúdo de tiol e as atividades de SOD e CAT e o nível de T4 no soro. Os resultados do presente estudo mostraram que a TQ protegeu contra deficiências de memória induzidas por PTU em ratos.

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“…The RAWM consisted of a black circular water-filled tank with six V-shaped stainless structures arranged to create six swim paths radiating out of an open central swim area (Gerges et al, 2004;Alzoubi et al, 2006). The training procedure consisted of a learning phase composed of 4 consecutive learning trials and a long-term memory test conducted 24 h after the last learning trial.…”

Section: Radial Arm Water Maze Proceduresmentioning

confidence: 99%

Chronic psychosocial stress accelerates impairment of long‐term memory and late‐phase long‐term potentiation in an at‐risk model of Alzheimer's disease

2011

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Although it is generally agreed that Aβ contributes to the pathogenesis of AD, its precise role in AD and the reason for the varying intensity and time of onset of the disease have not been elucidated. In addition to genetic factors, environmental issues such as stress may also play a critical role in the etiology of AD. This study examined the effect of chronic psychosocial stress in an at-risk (treatment with a subpathogenic dose of Aβ; "subAβ") rat model of AD on long-term memory by three techniques: memory tests in the radial arm water maze, electrophysiological recordings of synaptic plasticity in anesthetized rats, and immunoblot analysis of learning- and long-term memory-related signaling molecules. Chronic psychosocial stress was induced using a rat intruder model. The subAβ rat model of AD was induced by continuous infusion of 160 pmol/day Aβ(1-42) via a 14-day i.c.v. osmotic pump. All tests showed that subAβ rats were not different from control rats. Result from behavioral tests and electrophysiological recordings showed that infusion of subAβ in chronically stressed rats (stress/subAβ group) caused significant impairment of cognitive functions and late-phase long-term potentiation (L-LTP). Molecular analysis of various signaling molecules after expression of L-LTP, revealed an increase in the levels of p-CREB in control, stress, and subAβ rats, but not in the stress/subAβ rats. These findings suggest that the chronic stress-induced molecular alteration may accelerate the impairment of cognition and synaptic plasticity in individuals "at-risk" for AD.

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Nicotine reverses adult‐onset hypothyroidism‐induced impairment of learning and memory: Behavioral and electrophysiological studies

Cited by 60 publications

References 73 publications

Acute nicotine treatment prevents rem sleep deprivation‐induced learning and memory impairment in rat

Acute nicotine treatment prevents rem sleep deprivation‐induced learning and memory impairment in rat

Thymoquinone reverses learning and memory impairments and brain tissue oxidative damage in hypothyroid juvenile rats

Chronic psychosocial stress accelerates impairment of long‐term memory and late‐phase long‐term potentiation in an at‐risk model of Alzheimer's disease

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