Nicotine modulates cognitive function in D-galactose-induced senescence in mice

Alireza Majdi, Saeed Sadigh-Eteghad*, Mahnaz Talebi, Fereshteh Farajdokht, Marjan Erfani, Javad Mahmoudi, Albert Gjedde

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

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Abstract

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.

Original languageEnglish
Article number194
JournalFrontiers in Aging Neuroscience
Volume10
ISSN1663-4365
DOIs
Publication statusPublished - 2018

Keywords

  • Aging
  • Learning and memory
  • Mitochondrial dysfunction
  • Neurotrophic factors
  • Nicotine
  • Oxidative stress

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