Cognitive Effects of Nicotine

Sofuoglu, Mehmet; Herman, Aryeh I.; Robinson, Cendrine; Waters, Andrew J.

doi:10.1016/b978-0-12-418679-8.00012-5

Cited by 4 publications

(3 citation statements)

References 142 publications

(160 reference statements)

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“…Nicotine (NIC, (S)-3-(1-methylpyrrolidin-2-yl)pyridine), the alkaloid found in tobacco leaves, promotes the function of ACh by binding to nAChRs in the brain and enhancing performance in several domains of cognitive functions, including attention, working memory, and learning [ 15 , 16 ]. Additionally, NIC reduces oxidative stress [ 17 ], suppresses neuroinflammation [ 18 ], and prevents the Aβ aggregation in the brain [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Anxiolytic, Promnesic, Anti-Acetylcholinesterase and Antioxidant Effects of Cotinine and 6-Hydroxy-L-Nicotine in Scopolamine-Induced Zebrafish (Danio rerio) Model of Alzheimer’s Disease

et al. 2021

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Cotinine (COT) and 6-hydroxy-L-nicotine (6HLN) are two nicotinic derivatives that possess cognitive-improving abilities and antioxidant properties in different rodent models of Alzheimer’s disease (AD), eluding the side-effects of nicotine (NIC), the parent molecule. In the current study, we evaluated the impact of COT and 6HLN on memory deterioration, anxiety, and oxidative stress in the scopolamine (SCOP)-induced zebrafish model of AD. For this, COT and 6HLN were acutely administered by immersion to zebrafish that were treated with SCOP before testing. The memory performances were assessed in Y-maze and object discrimination (NOR) tasks, while the anxiety-like behavior was evaluated in the novel tank diving test (NTT). The acetylcholinesterase (AChE) activity and oxidative stress were measured from brain samples. The RT-qPCR analysis was used to evaluate the npy, egr1, bdnf, and nrf2a gene expression. Our data indicated that both COT and 6HLN attenuated the SCOP-induced anxiety-like behavior and memory impairment and reduced the oxidative stress and AChE activity in the brain of zebrafish. Finally, RT-qPCR analysis indicated that COT and 6HLN increased the npy, egr1, bdnf, and nrf2a gene expression. Therefore, COT and 6HLN could be used as tools for improving AD conditions.

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Section: Introductionmentioning

confidence: 99%

Anxiolytic, Promnesic, Anti-Acetylcholinesterase and Antioxidant Effects of Cotinine and 6-Hydroxy-L-Nicotine in Scopolamine-Induced Zebrafish (Danio rerio) Model of Alzheimer’s Disease

et al. 2021

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“…Nicotine (NIC) is an alkaloid extracted from Nicotiana tabacum and an exogenous agonist of nAChRs [ 15 ]. Accumulated evidence from animal and clinical studies showed that NIC has cognitive-enhancing effects, improving performance in several domains of cognition, including attention, learning, and working memory [ 16 ]. Moreover, NIC acts as an antioxidant, reducing the oxidative stress [ 17 ], has anti-inflammatory effects [ 18 ], and is neuroprotective against Aβ, reducing its aggregation in the brain [ 19 ].…”

Section: Introductionmentioning

confidence: 99%

Cotinine and 6-Hydroxy-L-Nicotine Reverses Memory Deficits and Reduces Oxidative Stress in Aβ25-35-Induced Rat Model of Alzheimer’s Disease

et al. 2020

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The nicotinic derivatives, cotinine (COT), and 6-hydroxy-L-nicotine (6HLN), showed promising cognitive-improving effects without exhibiting the nicotine’s side-effects. Here, we investigated the impact of COT and 6HLN on memory impairment and the oxidative stress in the Aβ25-35-induced rat model of Alzheimer’s disease (AD). COT and 6HLN were chronically administered to Aβ25-35-treated rats, and their memory performances were assessed using in vivo tasks (Y-maze, novel object recognition, and radial arm maze). By using in silico tools, we attempted to associate the behavioral outcomes with the calculated binding potential of these nicotinic compounds in the allosteric sites of α7 and α4β2 subtypes of the nicotinic acetylcholine receptors (nAChRs). The oxidative status and acetylcholinesterase (AChE) activity were determined from the hippocampal tissues. RT-qPCR assessed bdnf, arc, and il-1β mRNA levels. Our data revealed that COT and 6HLN could bind to α7 and α4β2 nAChRs with similar or even higher affinity than nicotine. Consequently, the treatment exhibited a pro-cognitive, antioxidant, and anti-AChE profile in the Aβ25-35-induced rat model of AD. Finally, RT-qPCR analysis revealed that COT and 6HLN positively modulated the bdnf, arc, and il-1β genes expression. Therefore, these nicotinic derivatives that act on the cholinergic system might represent a promising choice to ameliorate AD conditions.

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“…Nicotine acts through specific nicotinic acetylcholine receptors and stimulates dopamine release thought to be responsible for the acute rewarding effect of nicotine. It increases the "reward cycle" effect of dopaminergic neurons in the anterior nicotine and increases the release of neurotransmitters such as acetylcholine, norepinephrine, dopamine and serotonin in the presynaptic region [2]. It is known that while acetylcholine causes an increase in performance and memory capacity, the release of dopamine and norepinephrine decreases pleasure and appetite [1].…”

Section: Introductionmentioning

confidence: 99%

Nicotine Dependence Level of University Students Relating to Type of Education and Gender

Doğanay¹,

Ozdemir²,

Trabzon³

2017

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Cognitive Effects of Nicotine

Cited by 4 publications

References 142 publications

Anxiolytic, Promnesic, Anti-Acetylcholinesterase and Antioxidant Effects of Cotinine and 6-Hydroxy-L-Nicotine in Scopolamine-Induced Zebrafish (Danio rerio) Model of Alzheimer’s Disease

Anxiolytic, Promnesic, Anti-Acetylcholinesterase and Antioxidant Effects of Cotinine and 6-Hydroxy-L-Nicotine in Scopolamine-Induced Zebrafish (Danio rerio) Model of Alzheimer’s Disease

Cotinine and 6-Hydroxy-L-Nicotine Reverses Memory Deficits and Reduces Oxidative Stress in Aβ25-35-Induced Rat Model of Alzheimer’s Disease

Nicotine Dependence Level of University Students Relating to Type of Education and Gender

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