title: [Effects of 90-day oral dimethoate exposure on glutamatergic system and neurobehavioral performance in rats].
abstract: OBJECTIVE
  To investigate the spatial learning and exploration along with the CNS excitatory amino acid neurotransmitters profiles in adult rats subchronically exposed to the anticholinesterase organophosphorus insecticide dimethoate.
  
  
  METHODS
  Rats were gavaged daily with dimethoate (0, 5, 10 or 20 mg/kg via oral) in NS. for 90 days. Morris water maze tasks were used to test the spatial learning and memory in the rats after the dimethoate exposure. Simultaneously, rats were decapitated for the determination of brain cholinesterase AChE activities, glutamate concentrations, and the NMDA receptor NMDA-R densities and affinities in hippocampus.
  
  
  RESULTS
  Latencies to find a hidden escape platform were significantly longer in dimethoate dosed groups than that of the control group in the place navigation tests. Subsequently, the times of crossing the location of platform which had been removed obviously decreased in the highest dose group compared with that of the control in the spatial probe tests (P < 0.05). AChE activity was significantly reduced 42% approximately 78% by all three doses of dimethoate (P < 0.05). Glutamate concentrations were increased significantly 132.9% approximately 134.5% by the two highest doses of dimethoate (P < 0.05). In addition, the NMDA receptor bindings were reduced 21.2% approximately 23.2% with the statistical significance at the same two highest doses (P < 0.05). Furthermore, the receptor affinities was reduced 33.1% by the highest dose group (P < 0.05). The lesions of spatial memory were statistically corrected with the decrease of the NMDA-R affinities (P < 0.05).
  
  
  CONCLUSIONS
  The cholinergic lesion as well as the excitatory amino acid system alteration might attribute to the inferior ability in spatial learning and memory in dimethoate subchronically exposed rats.
authors.affiliation: Key Laboratory of Public Health and Safety, Ministry of Education, School of Public Health, Fudan University, Shanghai 200032, China.
authors.forename: Qiang-en
authors.initials: QE
authors.lastname: Wu
authors.forename: Xin-min
authors.initials: XM
authors.lastname: Yao
authors.forename: Ting-ting
authors.initials: TT
authors.lastname: Ban
authors.forename: Nan
authors.initials: N
authors.lastname: Jiang
authors.forename: Chun-feng
authors.initials: CF
authors.lastname: Shao
authors.forename: Xiu-li
authors.initials: XL
authors.lastname: Chang
authors.forename: Zhi-jun
authors.initials: ZJ
authors.lastname: Zhou
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D002908:Chronic Disease; D004117:Dimethoate / Q000633:toxicity*; D004195:Disease Models, Animal; D018698:Glutamic Acid / Q000378:metabolism*; D007306:Insecticides / Q000633:toxicity; D007858:Learning / Q000187:drug effects*; D008297:Male; D008568:Memory / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D059550:Toxicity Tests, Subchronic
chemical_list: D007306:Insecticides; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D000110:Acetylcholinesterase; D004117:Dimethoate