Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in Mice
Here, we tested the claim that nicotine attenuates the signs of brain dysfunction in the model of brain aging induced by D-galactose (DGal) in mice. We administered nicotine at doses of 0.1, 0.5 and 1 mg/kg by the subcutaneous (s.c.) or at 0.1 mg/kg by the intranasal (i.n.) routes in mice that had r...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2018-07-01
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| Series: | Frontiers in Aging Neuroscience |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/article/10.3389/fnagi.2018.00194/full |
| _version_ | 1828497000355594240 |
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| author | Alireza Majdi Saeed Sadigh-Eteghad Mahnaz Talebi Fereshteh Farajdokht Marjan Erfani Javad Mahmoudi Albert Gjedde Albert Gjedde Albert Gjedde Albert Gjedde Albert Gjedde |
| author_facet | Alireza Majdi Saeed Sadigh-Eteghad Mahnaz Talebi Fereshteh Farajdokht Marjan Erfani Javad Mahmoudi Albert Gjedde Albert Gjedde Albert Gjedde Albert Gjedde Albert Gjedde |
| author_sort | Alireza Majdi |
| collection | DOAJ |
| description | Here, we tested the claim that nicotine attenuates the signs of brain dysfunction in the model of brain aging induced by D-galactose (DGal) in mice. We administered nicotine at doses of 0.1, 0.5 and 1 mg/kg by the subcutaneous (s.c.) or at 0.1 mg/kg by the intranasal (i.n.) routes in mice that had received DGal at the dose of 500 mg/kg subcutaneous (s.c.) for 6 weeks. We assessed animal withdrawal signs as the number of presented somatic signs, thermal hyperalgesia, elevated plus maze (EPM) and open field tests. We evaluated spatial memory and recognition with Barnes maze and novel object recognition (NOR) tests. We tested brain tissue for reactive oxygen species (ROS), mitochondrial membrane potential, caspase-3, Bax, Bcl-2, cytochrome C, brain-derived neurotrophic factor and nerve growth factor levels. Nicotine administration in model groups (0.5 mg/kg s.c. and 0.1 mg/kg i.n. doses) significantly attenuated impairment of spatial and episodic memories in comparison to normal saline-received model group. These doses also reduced mito-oxidative damage as well as apoptosis and raised neurotrophic factors level in model groups in comparison to normal saline-received model group. The 1 mg/kg s.c. dose nicotine revealed withdrawal signs compared with the other nicotine-received groups. Nicotine at specific doses and routes has the potential to attenuate age-related cognitive impairment, mito-oxidative damage, and apoptosis. The doses raise neurotrophic factors without producing withdrawal signs. |
| first_indexed | 2024-12-11T12:40:46Z |
| format | Article |
| id | doaj.art-c7b5c89397cf42fbb2fa970d9b3be311 |
| institution | Directory Open Access Journal |
| issn | 1663-4365 |
| language | English |
| last_indexed | 2024-12-11T12:40:46Z |
| publishDate | 2018-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Aging Neuroscience |
| spelling | doaj.art-c7b5c89397cf42fbb2fa970d9b3be3112022-12-22T01:07:00ZengFrontiers Media S.A.Frontiers in Aging Neuroscience1663-43652018-07-011010.3389/fnagi.2018.00194343764Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in MiceAlireza Majdi0Saeed Sadigh-Eteghad1Mahnaz Talebi2Fereshteh Farajdokht3Marjan Erfani4Javad Mahmoudi5Albert Gjedde6Albert Gjedde7Albert Gjedde8Albert Gjedde9Albert Gjedde10Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, IranNeurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, IranDepartments of Clinical Research and Nuclear Medicine, Odense University Hospital, University of Southern Denmark, Odense, DenmarkDepartment of Neuroscience, University of Copenhagen, Copenhagen, DenmarkDepartment of Neurology and Neurosurgery, McGill University, Montreal, QC, CanadaDepartment of Radiology and Radiological Science, Johns Hopkins University, Baltimore, MD, United StatesHere, we tested the claim that nicotine attenuates the signs of brain dysfunction in the model of brain aging induced by D-galactose (DGal) in mice. We administered nicotine at doses of 0.1, 0.5 and 1 mg/kg by the subcutaneous (s.c.) or at 0.1 mg/kg by the intranasal (i.n.) routes in mice that had received DGal at the dose of 500 mg/kg subcutaneous (s.c.) for 6 weeks. We assessed animal withdrawal signs as the number of presented somatic signs, thermal hyperalgesia, elevated plus maze (EPM) and open field tests. We evaluated spatial memory and recognition with Barnes maze and novel object recognition (NOR) tests. We tested brain tissue for reactive oxygen species (ROS), mitochondrial membrane potential, caspase-3, Bax, Bcl-2, cytochrome C, brain-derived neurotrophic factor and nerve growth factor levels. Nicotine administration in model groups (0.5 mg/kg s.c. and 0.1 mg/kg i.n. doses) significantly attenuated impairment of spatial and episodic memories in comparison to normal saline-received model group. These doses also reduced mito-oxidative damage as well as apoptosis and raised neurotrophic factors level in model groups in comparison to normal saline-received model group. The 1 mg/kg s.c. dose nicotine revealed withdrawal signs compared with the other nicotine-received groups. Nicotine at specific doses and routes has the potential to attenuate age-related cognitive impairment, mito-oxidative damage, and apoptosis. The doses raise neurotrophic factors without producing withdrawal signs.https://www.frontiersin.org/article/10.3389/fnagi.2018.00194/fullagingnicotinelearning and memoryoxidative stressmitochondrial dysfunctionneurotrophic factors |
| spellingShingle | Alireza Majdi Saeed Sadigh-Eteghad Mahnaz Talebi Fereshteh Farajdokht Marjan Erfani Javad Mahmoudi Albert Gjedde Albert Gjedde Albert Gjedde Albert Gjedde Albert Gjedde Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in Mice Frontiers in Aging Neuroscience aging nicotine learning and memory oxidative stress mitochondrial dysfunction neurotrophic factors |
| title | Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in Mice |
| title_full | Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in Mice |
| title_fullStr | Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in Mice |
| title_full_unstemmed | Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in Mice |
| title_short | Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in Mice |
| title_sort | nicotine modulates cognitive function in d galactose induced senescence in mice |
| topic | aging nicotine learning and memory oxidative stress mitochondrial dysfunction neurotrophic factors |
| url | https://www.frontiersin.org/article/10.3389/fnagi.2018.00194/full |
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