List of Articles Catalepsy

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  1 - Evaluation of anti-cataleptic effect of Levodopa-Carbidopa and sertraline in the parkinsonian rats
  سیامک ریحانی راد جواد محمودی مجید خانمحمدی شلاله گنجی پیام سیفی
  Long-term administration of Levodopa in parkinsonian patients leads to development of somemotor disorders such as L-dopa induced dyskinesia and off-phenomena. Hence employment ofstrategy for effective treatment of this disease is of interest.In this investigation we att More

  Long-term administration of Levodopa in parkinsonian patients leads to development of somemotor disorders such as L-dopa induced dyskinesia and off-phenomena. Hence employment ofstrategy for effective treatment of this disease is of interest.In this investigation we attempted toevaluate the effect of sertraline on anti-cataleptic effect of L-dopa in 6-hydroxydopamine (6-OHDA) lesioned rats. Catalepsy was induced by infusion of 6-OHDA (8μg/2μl/rat) into theSubstantia nigra. These rats received intraperitoneally (i.p.) L-Dopa (15mg/kg) twice daily for20 consecutive days, and anti-cataleptic effect of L-dopa was evaluated by bar-test on days 5,10, 15 and 20. The results present that L-dopaexert anti-cataleptic effect only until day 15, andits effect was vanished on the day 20. On the day 21, these rats co-injected with three differentdoses of sertraline (0.5, 1and 2mg/kg, i.p.) and L-dopa (15mg/kg, ip). Sertralineat the dose of 2mg/kg improved the anti-cataleptic effect of L-dopa. Furthermore, the effect of sertraline (2mg/kg, i.p.) on anti-cataleptic effect of L-dopa (15mg/kg, ip) was antagonised by NAN-190 (0.5mg/kg, i.p.) as a 5-HT1A receptor antagonist. Theseresults showed that sertraline improvestheanti-cataleptic effect of L-dopa in the 6-OHDA-lesioned rats and probably this effect mediatedthrough activation of 5HT1A receptors. Manuscript profile
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  2 - Role of Adenosine A2A receptors on 6-Hydroxydopmaine-induced catalepsy in rats
  S. Reyhani-Rad, J. Mahmoudi,
  Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease in ageingindividuals. This movement disorder caused by degeneration of dopaminergic neurons from thesubstantia nigra pars compacta (SNc). Caffeine consumption has been proposed to be a More

  Parkinson’s disease (PD) is the second most prevalent neurodegenerative disease in ageingindividuals. This movement disorder caused by degeneration of dopaminergic neurons from thesubstantia nigra pars compacta (SNc). Caffeine consumption has been proposed to be associatedwith a reduced risk of Parkinson’s disease and caffeine in rodent models has protective effects.We have shown that caffeine and SCH58261 as A2A receptor antagonists improve motordysfunctions induced by 6-hydroxydopamine (animal model of Parkinson’s disease) in rats. Thepresent study extends these findings by investigating the role of A2A receptors on motor disorderinduced by unilateral infusion of 6-OH-dopamine into the substantia nigra, compact part (SNc)in rat. The experimental study was carried out on 72 male Wistar rats weighing between 180-200 g. Animals were divided into the groups contain 8 rats per group and were kept in standardcondition. 6-OHDA-induced catalepsy was assessed by using bar test. Caffeine (30 mg/kg i.p.)attenuated catalepsy on bar test in parkinsonian rats (P<0.001), whereas with dose of 10 mg/kgdid not produce significant effect (P>0.05). SCH58261 (2 mg/kg i.p) significantly improvedcatalepsy in bar test (P<0.001) in parkinsonian rat. These findings suggest that A2A receptors areinvolved in 6-OHDA-induced motor deficit like catalepsy. It seems that attenuating of catalepsymay caused by inhibition of A2A receptors. Manuscript profile
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  3 - The effect of caloric restriction on reserpine-induced catalepsy in rats model of Parkinson's disease
  Azam Khalaj Tahreh sadat Shobeiri Mohammad Reza Yazdian
  Aim and Background: Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease and the most common cause of disability . it is a progressive disease that is associated with the destruction of nerve cells. Caloric restriction is th More

  Aim and Background: Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease and the most common cause of disability . it is a progressive disease that is associated with the destruction of nerve cells. Caloric restriction is the only preventive action that has a life long-lasting effect on laboratory models. It has been shown in a large scale of laboratory animals that caloric restriction increases life expectancy, decreases the incidence of several age-related diseases, and preserves youth activities. Therefore, the aim of this study was to investigate the effect of caloric restriction diet on reserpine-induced catalepsy in male rats model of Parkinson's disease. Material and Methods: In this study, 30 Wistar rats were divided in 5 groups (control, Parkinson's disease,caloric restriction, Parkinson's disease + caloric restriction, caloric restriction+ Parkinson's disease(2) ).Animals in caloric restriction groups were under the caloric restriction of 30 percent. Parkinson's disease was induced by administration of Reserpine (1 mg/kg, i.p). The bar- test was used to measure cataleptic symptoms. Results: catalepsy was significantly lower in of caloric restriction + Parkinson's disease and caloric restriction+ Parkinson's disease (2) groups than in Parkinson's disease group. (P <0/05). Conclusion: caloric restriction of 30 percent can improve reserpine-induced catalepsy in male rats model of Parkinson's disease. Also, caloric restriction before inducing Parkinson's disease reduces the severity of complications after getting sick, including catalepsy. Manuscript profile
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  4 - The Pycnogenol Improves Motor Function and Anxiety Behavior in 6-hydroaydoamine (6-OHDA)-induced Experimental Model of Parkinson’s Disease in NMRI Male Mice
  Farajollah Jafari Mahdi Goudarzvand Ramin Hajikhani Mostafa Qorbani Jalal Solati
  10.22034/ascij.2021.684779
  Considering the role of oxidants in the pathogenesis of this disease, in this study, the effect of pycnogenol as an antioxidant on the improvement of motor function and anxiety behavior in the experimental model of Parkinson’s disease were assessed. Forty male NMR More

  Considering the role of oxidants in the pathogenesis of this disease, in this study, the effect of pycnogenol as an antioxidant on the improvement of motor function and anxiety behavior in the experimental model of Parkinson’s disease were assessed. Forty male NMRI mice were randomly divided into five groups (n=8 in each group): The control (saline) unilaterally received 3 μl of normal saline solution containing 0.1% ascorbic acid, as a solvent of 6-hydroxy dopamine (6-OHDA), into the left strianum. The treatment group received 6-OHDA toxin containing 1% ascorbic acid at a rate of 3 µg/µl in the left striatum and then received the distilled water, as pycnogenol solvent, via gavage for 7 days (the lesion group). The pycnogenol-treated groups received pycnogenol at doses of 10, 20, and 30 mg/kg via gavage for 7 days. The animals were stereotaxically operated to inject 6-OHDA toxin into the left striatum. Seven days after induction of Parkinson’s model, apomorphine was intraperitoneally used at dose of 0.5 mg/kg and the number of rotation of the animals was measured to confirm the damage to neurons in the striatum. Besides, the catalepsy or muscle stiffness by the bar test and the anxiety behavior by the plus maze test (EPM) were measured. The total number of rotations in apomorphine test showed a significant decrease in the groups receiving pycnogenol. Moreover, administration of pycnogenol significantly reduced catalepsy in pycnogenol-treated groups. The result of the anxiety behavior test demonstrated that the percentage of open arm time (OAT) and the number of open and close arm entries, as an indicator of the animal’s locomotor activity, significantly increased in the pycnogenol-treated groups. Pycnogenol with its antioxidant effect ameliorates movement deficit and reduces anxiety behavior in animal model of Parkinson’s disease.. Manuscript profile
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  5 - The Effect of Cinnamon Extract (Cinnamum zeylanicum) on Catalepsy in Male Mice Model of Parkinson's Disease
  M. Mohammad Ali Mansouri A.A. Moazedi G.A. Parham
  Catalepsy or muscle rigidity is a neurological disease characterized by muscle stiffness or rigidity of muscles, organs decreased sensitivity to pain and stability regardless of external stimuli-known and one of the main symptoms of Parkinson's disease is considered. Du More

  Catalepsy or muscle rigidity is a neurological disease characterized by muscle stiffness or rigidity of muscles, organs decreased sensitivity to pain and stability regardless of external stimuli-known and one of the main symptoms of Parkinson's disease is considered. Due to the increasing levels of acetylcholine in the brain, treatment is focused on the use of muscarinic receptor antagonists. Despite relieve the symptoms, there are severe side effects. In this study, the effect of cinnamon extract on catalepsy in mice model of Parkinson's disease was conducted. Overall, 70 male mice (30 ± 2 g) were randomly divided into seven groups: control group, rotenone solvent, rotenone group and 4 groups of rotenone, subsequent doses 100, 200, 400 and 600 mg/kg cinnamon extract. To create models of Parkinson's disease, rotenone (2 mg/kg/ 48 h) was administered for 19 d and creating models of Parkinson's disease was evaluated. After verification of the model, different doses of cinnamon for 20 d (every 48 h) were injected intraperitoneally (IP). The effects of cinnamon extract on catalepsy was compared with other groups and the results were analyzed by ANOVA and Tukey test.  PP<0.05). Cinnamon could reduce catalepsy in mice models of Parkinson's disease, probably due to antioxidant compounds and flavonoids and the impact of these compounds on the nervous system. Manuscript profile