Neuronal Nitric Oxide Inhibitor 7-Nitroindazole Improved Brain-Derived Neurotrophic Factor and Attenuated Brain Tissues Oxidative Damage and Learning and Memory Impairments of Hypothyroid Juvenile Rats

Memarpour, Sara; Beheshti, Farimah; Baghcheghi, Yousef; Vafaei, Abbas Ali; Hosseini, Mahmoud; Rashidy-Pour, Ali

doi:10.1007/s11064-020-03128-6

Cited by 22 publications

(9 citation statements)

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“…According to the biochemical results of the present study, higher MDA level was observed in both hippocampal and cortical tissues of hypothyroid rats compared to the control ones while SOD activity and total thiol content were signi cantly abated. These data are compatible with the previous investigations indicating the correlation between oxidative stress status in the hippocampus and learning and memory impairments due to hypothyroidism (17,49). Growing body of research has shown that low levels of THs are followed by production of free radicals in the cell in a variety of ways which are associated with changes in mitochondrial activity and respiratory chain that ultimately recognized as a well-known role in the oxidative status (9).…”

Section: Discussionsupporting

confidence: 92%

Treatment by Vitamin D Reversed the Adverse Effects of Hypothyroidism on Learning and Memory in Juvenile Rats: Protection Against Acetylcholinesterase Activity and Brain Tissue Oxidative Damage.

Rastegar-Moghaddam

Alipour

Rajabian

et al. 2021

Preprint

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Apart from a role as a key regulator of calcium/phosphate homeostasis, vitamin D (Vit D) is suggested to be a potential player in nervous system growth and function. This study aimed to assess the impacts of Vit D administration against memory impairment, oxidative damage and acetylcholinesterase (AchE) overactivity caused by hypothyroidism in juvenile rats. The animals were randomly grouped as: 1) Control; 2) Hypothyroid; 3) Hypothyroid-Vit D 100 and 4) Hypothyroid-Vit D 500. Propylthiouracil (PTU) was added to their drinking water (0.05%) for 6 weeks and Vit D (100 or 500 IU/kg) treatment was daily performed by gavage. Morris water maze (MWM) and passive avoidance (PA) tests were performed. The brains were removed under deep anesthesia, then the hippocampal and cortical tissues were separated to assess biochemical parameters. Hypothyroidism was significantly associated with learning and memory impairment in MWM and PA tests. Hypothyroidism also elevated acetylcholinesterase (AChE) activity and malondialdehyde (MDA) content, while it reduced thiol content and superoxide dismutase (SOD) activity in the brain. Treatment with Vit D recovered hypothyroidism-induced cognitive impairment and improved memory performance in MWM and PA tasks. On the other hand, Vit D alleviated AChE activity and MDA level, whereas increased SOD activity and thiol content in the hippocampal and cortical tissues. In conclusion, these outcomes suggest that oral consumption of Vit D may play a protective role against memory dysfunction caused by hypothyroidism by inhibiting AChE activity and oxidative stress in the brain.

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Section: Discussionsupporting

confidence: 92%

Treatment by Vitamin D Reversed the Adverse Effects of Hypothyroidism on Learning and Memory in Juvenile Rats: Protection Against Acetylcholinesterase Activity and Brain Tissue Oxidative Damage.

Rastegar-Moghaddam

Alipour

Rajabian

et al. 2021

Preprint

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“…It is also known that oxidative damage in the brain may lead to cognitive impairments, and hypothyroidism-induced oxidative stress in the brain has been reported to contribute to learning and memory deficits. Additionally, a negative association between oxidative stress and BDNF levels has been shown [30]. However, in our experimental conditions, in both individual models and in the model of the co-occurrence of hypothyroidism and endogenous depression, this pathway does not seem to be directly or indirectly affected because we did not observe any changes in markers of oxidative stress (MDA and 4-HNE) or hippocampal BDNF and NGF expression, which suggests that learning and memory impairment does not occur through oxidative stress induction.…”

Section: Discussionmentioning

confidence: 97%

Contribution of Hypothyroidism to Cognitive Impairment and Hippocampal Synaptic Plasticity Regulation in an Animal Model of Depression

Głombik

Detka

Bobula

et al. 2021

IJMS

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The role that thyroid hormone deficiency plays in depression and synaptic plasticity in adults has only begun to be elucidated. This paper analyzes the possible link between depression and hypothyroidism in cognitive function alterations, using Wistar–Kyoto (WKY—an animal model of depression) rats and control Wistar rats under standard and thyroid hormone deficiency conditions (propylthiouracil administration—PTU). A weakening of memory processes in the WKY rats is shown behaviorally, and in the reduction of long-term potentiation (LTP) in the dentate gyrus (DG) and CA1 hippocampal regions. PTU administration decreased LTP and increased basal excitatory transmission in the DG in Wistar rats. A decrease in short-term synaptic plasticity is shown by the paired-pulse ratio measurement, occurring during hypothyroidism in DG and CA1 in WKY rats. Differences between the strains may result from decreases in the p-CaMKII, p-AKT, and the level of acetylcholine, while in the case of the co-occurrence of depression and hypothyroidism, an increase in the p-ERK1-MAP seemed to be important. Obtained results show that thyroid hormones are less involved in the inhibition of glutamate release and/or excitability of the postsynaptic neurons in WKY rats, which may indicate a lower sensitivity of the hippocampus to the action of thyroid hormones in depression.

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“…The brain is very susceptible to hypothyroidism-associated damage (Figueroa et al, 2021;Arianas et al, 2022). It was also previously reported that learning and memory impairments due to hypothyroidism in immature rats were accompanied by apoptosis in the hippocampus and reduction in ki67 content as a marker of neurogenesis (Baghcheghi et al, 2018;Baghcheghi et al, 2019;Alikhani et al, 2020;Baghcheghi et al, 2020;Memarpour et al, 2020).…”

Section: Discussionmentioning

confidence: 90%

“…These effects were accompanied by learning and memory impairments (Farrokhi et al, 2014;Hosseini et al, 2010a;Beheshti et al, 2017a;Beheshti et al, 2017b). It was also reported that hypothyroidism induced by propylthiouracil (PTU) in immature rats was followed by learning and memory impairments when the rats were examined after 6 weeks (Baghcheghi et al, 2018;Baghcheghi et al, 2019;Memarpour et al, 2020), which was accompanied by apoptosis in the hippocampus (Baghcheghi et al, 2020) and reduction in ki67 content as a marker of neurogenesis (Alikhani et al, 2020). The mechanism(s) involved in hypothyroidism-associated brain injury has been widely investigated.…”

Section: Introductionmentioning

confidence: 99%

The effects of curcumin in learning and memory impairment associated with hypothyroidism in juvenile rats: the role of nitric oxide, oxidative stress, and brain-derived neurotrophic factor

Ahmadabady

Hosseini

Shafei

et al. 2022

Behavioural Pharmacology

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The effect of curcumin (Cur) on cognitive impairment and the possible role of brain tissue oxidative stress, nitric oxide (NO) levels, and brain-derived neurotrophic factor (BDNF) were investigated in juvenile hypothyroid rats. The juvenile rats (21 days old) were allocated into the following groups: (1) control; (2) hypothyroid (0.05% propylthiouracil (PTU) in drinking water); (3–5) hypothyroid-Cur 50, 100, and 150, which in these groups 50, 100, or 150 mg/kg, Cur was orally administered by gavage during 6 weeks. In the hypothyroid rats, the time elapsed and the traveled distance to locate the hidden platform in the learning trials of Morris water maze (MWM) increased, and on the probe day, the amount of time spent in the target quadrant and the distance traveled in there was decreased. Hypothyroidism also decreased the latency and increased the time spent in the darkroom of the passive avoidance (PA) test. Compared with the hypothyroid group, Cur enhanced the performance of the rats in both MWM and PA tests. In addition, Cur reduced malondialdehyde concentration and NO metabolites; however, it increased thiol content as well as the activity of catalase (CAT) and superoxide dismutase enzymes in both the cortex and hippocampus. Cur also increased hippocampal synthesis of BDNF in hypothyroid rats. The beneficial effects of Cur cognitive function in juvenile hypothyroid rats might be attributed to its protective effect against oxidative stress and potentiation of BDNF production.

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Neuronal Nitric Oxide Inhibitor 7-Nitroindazole Improved Brain-Derived Neurotrophic Factor and Attenuated Brain Tissues Oxidative Damage and Learning and Memory Impairments of Hypothyroid Juvenile Rats

Cited by 22 publications

References 50 publications

Treatment by Vitamin D Reversed the Adverse Effects of Hypothyroidism on Learning and Memory in Juvenile Rats: Protection Against Acetylcholinesterase Activity and Brain Tissue Oxidative Damage.

Treatment by Vitamin D Reversed the Adverse Effects of Hypothyroidism on Learning and Memory in Juvenile Rats: Protection Against Acetylcholinesterase Activity and Brain Tissue Oxidative Damage.

Contribution of Hypothyroidism to Cognitive Impairment and Hippocampal Synaptic Plasticity Regulation in an Animal Model of Depression

The effects of curcumin in learning and memory impairment associated with hypothyroidism in juvenile rats: the role of nitric oxide, oxidative stress, and brain-derived neurotrophic factor

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