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1.
DARU-Journal of Pharmaceutical Sciences. 2011; 19 (5): 338-343
in English | IMEMR | ID: emr-116695

ABSTRACT

In Parkinson_s disease [PD] prolong use of L-DOPA causes some motor disorders such as wearing-off and L-DOPA induced dyskinesia [LID]. In this investigation the effect of 8-OHDAPT, as a 5-HT[1A] agonist on anti-cataleptic effect of L-DOPA in 6-hydroxydopamine [6-OHDA] lesioned male Wistar rats was investigated. Catalepsy was induced by unilateral injection of 6-OHDA [8 micro g/2 micro l/rat] into the central region of the SNc. After 3 weeks as a recovery period, animals received intraperitoneally [i.p.] L-DOPA [15 mg/kg] twice daily for 20 days, and anti-cataleptic effect of L-DOPA was assessed by bar-test at days of 5, 10, 15 and 20. The results showed that L-DOPA had anti-cataleptic effect only until the day of 15, and its effect was decreased on the day of 20. On the day of 21, rats were co-injected with three different doses of 8-OHDAPT [0.1, 0.5 and 2.5 mg/kg, i.p.] and L-DOPA [15 mg/kg, ip]. 8-Hydroxy-2-[di-n-propylamino] tetralin [8-OHDAPT] improved anti-cataleptic effect of L-DOPA at the dose of 0.5 mg/kg. Moreover the effect of 8-OHDAPT on anti-cataleptic effect of L-DOPA [15 mg/kg, ip] was abolished by 1-[2-methyoxyphenyl]-4-[4-[2-phthalamido] butyl] piperazine hydrobromide [NAN-190; 0.5 mg/kg, i.p.] as a 5-HT[1A] receptor antagonist. According to the obtained results, it may be concluded that activation of 5-HT[1A] receptors by 8-OHDAPT may improve anti-cataleptic effect of L-DOPA in a 6-OHDA- induced rat model of PD. Further studies are required to clarify the exact mechanism of interaction between 5-HT[1A] and dopaminergic neurons

2.
Journal of Zanjan University of Medical Sciences and Health Services. 2007; 15 (59): 35-44
in Persian | IMEMR | ID: emr-112615

ABSTRACT

Increased level of dopamine in accumbens nucleus has a key role in the rewarding effects or positive reinforcement of abused drugs, whereas serotonin facilitates dopamine release in brain .The aim of this study was to investigate the effect of concurrent use of amantadine and paroxetine on reinforcing effect of morphine in conditioned place preference model in mice. In this experimental study male NMRI mice [20-30 g] were used within 6 consecutive days including preconditioning, conditioning and postconditioning phases. On the first day, after removal of the partitions, time spent in every 3 compartments was measured for 10 minutes. After determination of low and high preferred side, animals received morphine sulfate [5 mg/kg] intraperitoneally on the 2nd and 4th days in the least preferred side, but on the 3rd and 5th days of the test, animals received saline [10ml/kg] in high preferred side. On the test day or postconditioning phase, animals received amantadine, and paroxetine alone or their concurrent does, instead of morphine. Control group received saline in both sides [n = 8]. Our results show that morphine significantly and dose dependently [2.5, 5,10 mg/kg] induced CPP [P<0.001]. Amantadine, only in doses of 5 and 10 mg /kg [P<0.01, P<0.001, respectively] induced CPP. Paroxetine induced CPP in all doses. Concurrent use of amantadine[10mg/kg] and paroxetine [10mg/kg] significantly enhances morphine - like CPP [P <0.001]. Concurrent use of drugs, releases dopamine and inhibit reuptake of serotonin, and may potentiate morphine-like CPP and could be useful in decreasing some opioid withdrawal signs


Subject(s)
Male , Animals, Laboratory , Paroxetine , Amantadine , Morphine , Mice , Substance-Related Disorders , Dopamine , Serotonin , Substance Withdrawal Syndrome
3.
Journal of Nursing and Midwifery Quarterly-Shaheed Beheshti University of Medical Sciences and Health Services. 2006; 16 (53): 39-46
in Persian | IMEMR | ID: emr-167393

ABSTRACT

Intravenous catheterization is one of the most common invasive procedures at hospitals. This practice is not devoid of complications. Phlebitis is a common complication. This clinical trial was conducted to compare between the efficacy of ethanol 70% and chlorhexidine 0.5% in ethanol 70% as disinfection solutions of the skin on the rate of catheter-related phlebitis. 80 hospitalized patients at emergency ward, CCU and post CCU were enrolled in the study and randomly assigned to one of two equal groups, i.e., for each group, a solution was used. All catheters were inserted and secured by the researcher in the same way. Insertion sites were observed every 12 hours for evidence of phlebitis according to Infusion Nursing Society Phlebitis Scale. Catheters were removed aseptically in the event of phlebitis or after 72 hours. The Study groups were matched in terms of age, sex, level of education, underlying disease and insertion site. Phlebitis occurred in 6 patients [15%] of the chlorhexidine group, and 15 patients [37.5%] of the ethanol group [P=0.022]. It can be concluded that disinfection by chlorhexidine may reduce the incidence of catheter-related phlebitis and can be routinely used in clinical practice

4.
IJMS-Iranian Journal of Medical Sciences. 1996; 21 (1-2): 3-10
in English | IMEMR | ID: emr-41113

ABSTRACT

The effects of dopamine D1 receptor antagonists [SCH 23390, +/- SKF 83566] and dopamine D2 receptor antagonists [haloperidol, sulpiride] on lithium-induced conditioned place aversion [CPA] in male rats and mice were investigated. Subcutaneous [SC] injection of different amounts of lithium induced CPA, dose-dependently. Serum lithium levels were related to the dose administered and were 0.34 +/- 0.02 to 1.49 +/- 0.03 mmol in rats and 0.26 +/- 0.02 to 1.36 +/- 0.08 mmol in mice. Pretreatment of the animals with SCH 23390 and +/- SKF 83566, and a non-selective dopamine receptor antagonist, chlorpromazine [CPZ], abolished lithium-induced CPA. Pretreatment of the rats with haloperidol and sulpiride, enhanced the lithium-induced CPA. Pretreatment of the animals with sulpiride enhanced the aversive effects of Li in both species. It is concluded that lithium-induced CPA is mediated through dopaminergic mechanisms, and the effects of Li and dopamine antagonists are not species dependent


Subject(s)
Dopamine Antagonists , Receptors, Dopamine , Receptors, Dopamine D1 , Receptors, Dopamine D2 , Rats , Mice
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