ABSTRACT
<p><b>OBJECTIVE</b>Numerous studies have described both motor defects and cognitive impairments in several strains of rodents following 3-nitropropionic acid (3-NP) intoxication. In the present study, we investigated spatial recognition memory in Kunming mice that just recovered from motor defects induced by 3-NP.</p><p><b>METHODS</b>Mouse model was made by systemic subacute 3-NP treatment, and spatial recognition memory was measured through the Y-maze Test, a simple two-trial recognition test.</p><p><b>RESULTS</b>(1) On day 15 following 3-NP treatment, affected Kunming mice did not show motor defects in the Rotarod test and presented normal gait again. (2) In the following Y-maze test after 1h interval, the percentage (90.0%) of mice showing novel arm preference in 3-NP treatment group was significantly higher than the random chance level (50%), although it was only slightly higher than that (83.3%) in control group. On day 45 after 3-NP treatment, mice failed to choose unfamiliar novel arm as first choice, and the same occured in the control group. (3) For both post-intoxicated (on day 15 and day 45 following 3-NP treatment) and control groups, the duration in the novel arm and the frequency of entering it, were longer and higher compared with familiar start and other arms. For these mice that recently recovered from motor defects following 3-NP intoxication, no spatial memory deficits were observed through Y-maze Test.</p><p><b>CONCLUSION</b>Kunming mice used in our assays might possess resistance to cognitive impairment induced by 3-NP, which is consistent with previous findings in Swiss EPM-M1 mice.</p>
Subject(s)
Animals , Male , Mice , Behavior, Animal , Convulsants , Toxicity , Maze Learning , Memory Disorders , Mice, Inbred Strains , Motor Activity , Movement Disorders , Nitro Compounds , Toxicity , Poisoning , Propionates , Toxicity , Recovery of Function , Physiology , Rotarod Performance Test , Time FactorsABSTRACT
Objective To explore the mechanism of deep brain stimulation(DBS)therapy to Parkinson's disease(PD).Methods We produced hemi-parkinsonian rat model with stereotaxically injecting 6-OHDA to right medial forebrain bundle(MFB)and stimulated ipsilateral subthalamu nucleus (STN)with platinum electrodes chronically to investigate the influence of DBS to the expression of Calbindin-28,synaptophysin and tyrosine dioxydase(TH)in Striatum by Western blot.In addition,slices of bilateral PD rats after DBS were stained to observe the expression of Calbindin-28 and synaptophysin in substantia nigra by Immunohistochemistry.Results High frequency stimulation impaired the rotational frequency 31% of unilateral PD rats triggered by apomophine;Long-term DBS increased the expression of TH in innocent striatum of unilateral PD rats 78.6%?9.5%,since the ipsilateral striatum(lesion side) was TH depleted by 6-OHDA insults;Calbindin-28 expression in ipsilateral striatum of hemi-PD rats raised up 75.4%?15.0% and long-term DBS reduced the effect by 43.0%?7.1%,meanwhile Calbindin-28 positive neurons in substantia nigra compacta in sham,PD and DBS rats were 74.5?10.2,75.7?15.6, 33.1?7.8.However,Synaptophysin expression in substantia nigra and striatum kept stable even after long- term DBS.Conclusions Consistent to the treatment to PD patients,DBS to STN alleviated the motor disorder of PD rats,the treatment might be based on regulating the expression of Calbindin-28 and TH.