title: Nicotine attenuates spatial learning deficits induced by sodium metavanadate.
abstract: Learning can be severely impaired as a consequence of exposure to environmental pollutants. Vanadium (V), a metalloid which is widely distributed in the environment, has been shown to exert toxic effects on a variety of biological systems including the nervous system. However, studies exploring the impact of vanadium on learning are limited. Herein, we investigated the effects of oral administration of sodium metavanadate (SMV) (15, 20 and 25mg/kg/day for 2weeks) on spatial learning using Morris water maze (MWM). Our results showed that pre-training administration of sodium metavanadate impaired learning in Morris water maze. Analyzing the role of cholinergic system in SMV-induced learning deficit, we found that bilateral intra-hippocampal infusion of nicotine (1μg/side) during training could significantly diminish the SMV-induced learning impairment. We next examined the expression of choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT) as cholinergic markers in CA1 region of hippocampus as well as in medial septal area (MSA). Our molecular analyses showed that vanadium administration decreased ChAT and VAChT protein expression, an effect that was attenuated by nicotine. Altogether, our results confirmed the toxic effects of SMV on spatial acquisition, while also pointing to the neuroprotective effects of nicotine on SMV-induced impairments in learning capabilities. These findings might open a new avenue for the prevention of vanadium adverse effects on spatial learning and memory through activation of cholinergic signaling pathway.
authors: Department of Pharmacology and Toxicology, Pharmaceutical Sciences Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
authors: Kian
authors: K
authors: Azami
authors: Kaveh
authors: K
authors: Tabrizian
authors: Rohollah
authors: R
authors: Hosseini
authors: Mohammad
authors: M
authors: Seyedabadi
authors: Marjan
authors: M
authors: Shariatpanahi
authors: Farshid
authors: F
authors: Noorbakhsh
authors: Abbas
authors: A
authors: Kebriaeezadeh
authors: Seyed Nasser
authors: SN
authors: Ostad
authors: Mohammad
authors: M
authors: Sharifzadeh
mesh_terms: D000284:Administration, Oral; D000704:Analysis of Variance; D000818:Animals; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004924:Escape Reaction / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism; D007859:Learning Disabilities / Q000139:chemically induced* / Q000188:drug therapy*; D008124:Locomotion / Q000187:drug effects; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D009538:Nicotine / Q000627:therapeutic use*; D018722:Nicotinic Agonists / Q000627:therapeutic use*; D011597:Psychomotor Performance / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D011930:Reaction Time / Q000187:drug effects; D013028:Space Perception / Q000187:drug effects* / Q000502:physiology; D013550:Swimming; D014638:Vanadates / Q000633:toxicity*; D050494:Vesicular Acetylcholine Transport Proteins / Q000378:metabolism
chemical_list: D018722:Nicotinic Agonists; D050494:Vesicular Acetylcholine Transport Proteins; D014638:Vanadates; D009538:Nicotine; D002795:Choline O-Acetyltransferase