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Showing 64 results for Mice

Mohammad Reza Zarrindast, Abolghasemi, Masoumeh Sabetkasai,
Volume 1, Issue 1 (4-1997)
Abstract

In the present study, the effects of different doses of nicotine on immobility time in mice were tested. Intraperitioneal administration of low doses of nicotine (0.025 mg/kg) decreased, but higher doses (0.8 and 1 mg/kg) increased immobility time. The anti-immobility response induced by low doses of nicotine was inhibited by high doses of the D2 receptor antagonist sulpiride, the central nicotinic receptor antagonist mecamylamine, reserpine and propranolol. The D1 receptor antagonist SCH 23390, the peripheral D2 receptor antagonist domperidone, hexamethonium, phenoxybenzamine and atropine did not alter nicotine effect. It can be concluded that the anti-immobility effect induced by low doses of nicotine is mediated by D2 dopamine receptor mechanism and possibly through a central nicotinic receptor stimulation.
Mohammad Reza Zarrindast, Marjan Pazouki, Shadi Nassiri-Rad,
Volume 2, Issue 1 (4-1998)
Abstract

  In this study, we investigated the effect of nicotinic receptor agonists and antagonists on the analgesic response to morphine in the formalin test. In experiments conducted in mice, nicotine produced an early dose-dependent analgesic effect. At a dose of 0.5 mg/kg, mecamylamine, a nicotinic receptor inhibitor, suppressed the analgesic effect induced by 0.1 mg/kg nicotine in both stages of the formalin test, while hexamethonium had no such effect. Atropine, a muscarinic receptor antagonist, reduced the nicotine response at doses of 5 and 10 mg/kg. Mecamylamine, hexamethonium and atropine had no effect on morphine-induced analgesia. Administered separately, the antagonists had no effect on the analgesic response either. High doses of mecamylamine lead to an increase of the pain response. We conclude that cholinergic and opioid receptors play a possible role in the analgesic effect induced by nicotine.



Volume 2, Issue 1 (4-1998)
Abstract

  There is evidence that sweeteners such as sucrose and saccharin interact with endogenous opioid systems. Further research has shown that feeding different concentrations of sucrose and saccharin alter latency in the tail-flick test. In this study, the influence of a 12-day regimen of different sweetening agents, sucrose (32%), saccharin (0.08%) and aspartame (0.16%) on morphine-induced analgesia in the formalin test was investigated. Male albino mice (20-27 g) were used for the experiments. The animals were given 12 days to adapt to the dietary conditions. An initial subcutaneous injection of saline or morphine (1.5, 3, 6 or 9 mg/kg) was given 30 minutes before the observation period. Recording of the early phase began immediately and continued for 10 minutes. Recording of the late response began 20 minutes after injection and continued for 10 minutes. Sucrose and aspartame increased the analgesia of morphine in the early phase while saccharin had no effect. On the other hand saccharin and sucrose decreased the effect of morphine in the late phase while aspartame increased the effect of morphine-induced analgesia. In conclusion, the present data provide further evidence for an important role of dietary variables in determining the effects of exogenous opioids on pain sensitivity.



Volume 2, Issue 1 (4-1998)
Abstract

  Numerous studies conducted in laboratory animals and humans indicate that angiotensin converting enzyme inhibitors reinforce memory and learning. In this paper we study the effect of injection of enalapril into the cerebral ventricles on spatial memory of white mice in the double- y maze, following the induction of an Alzheimer- like amnestic model with scopolamine. To estimate the duration of working memory, the adaptive response method was used following a temporal pause. Animals completing the training period were injected with 2.5 mg intraperitoneal scopolamine. Injection of this dose that was determined by the dose-response curve led to a significant decrease in the percentage of correct responses of working memory (p<0.01), without any effect on reference memory. Response delay time significantly increased in both types of memory (p<0.01). Therefore, an Alzheimer-like amnestic model was induced by this dose with a relatively isolated effect on current memory. Following induction of this amnestic model in mice, the effects of 3, 5 and 10 µg injections of enalapril on the percentage of correct responses and delay time were measured without pause and also by the adaptive response method with 5 and 30 second pauses. Enalapril led to an increase in correct responses of working memory in all doses without pause (p<0.01), while this effect was only observed at 3 and 10 µg doses of enalapril with pause (p<0.05). Enalapril led to a decrease in response delay in both types of memory (p<0.05). Considering these results and previous studies, it seems that enalapril blocks the inhibitory effect of endogenous angiotensin II on the cholinergic memory centers, and thereby leads to a reinforcement of memory, especially working memory.



Volume 2, Issue 2 (11-1998)
Abstract

The effects of caerulin, a CCK receptor agonist, and proglumide, a receptor antagonist, on hyperalgesia induced by sciatic nerve ligation, was studied in mice. Tolerance to the morphine response was obtained 3,7, 14,21 and 28 days after unilateral sciatic nerve ligation. Maximum hyperalgesia was found 14 days after nerve ligation. Caerulin increased morphine antinociception in nerve-ligated animals. The drug also induced antinociception in intact animals. Proglumide also induced antinociception in nerve-ligated mice. The antagonist increased the morphine response but did not alter the effect of caerulin. We conclude that the CCK receptor mechanism may have a role in hyperalgesia induced by nerve ligation
Hedayat Sahrai, Mohammad Reza Shariati, Hasan Aghai-Firoozabadi, Ali Khoshbaten, Alireza Asgari, Hasan Ghoshooni,,
Volume 2, Issue 2 (11-1998)
Abstract

  The involvement of nitric oxide (NO) in the reinforcing properties of opioids was studied by examining the effect of a NO precursor (L-arginine) and NO synthase inhibitor (L-nitro-amino-methyl-ester, L-NAME) on the conditioned place preference (CPP) induced by morphine. The experiment was performed on male albino Swiss- White mice (25 ± 5 g). L-arginine in doses of 100, 200 and 500 mg/kg (i.p.) decreased CPP significantly, while L-arginine induced CPP in doses of 200 and 500 mg/kg per se. L-NAME doses of 0.75, 1.25, 2.5, 5, 10, 20 and 300 mg/kg (i.p.)had no effect on CPP induced by morphine, but injection of L-NAME (5 mg/kg) significantly decreased the effect of L-arginine on morphine-induced CPP. Therefore it may be concluded that NO may be involved in the psychological dependence to morphine.

 



Volume 2, Issue 2 (11-1998)
Abstract

  To detect the effects of sympathomimetic drugs with selective action on β1 and β2 adrenoceptors, male albino mice were treated by intraperitoneal administration of dobutamine and terbutaline for 15 days. Three groups of mice were selected as dobutamine, terbutaline and control groups, respectively. At the end of the experiment, the animals were sacrificed and the parotid glands were removed and prepared for biochemical studies. The two drugs induced an increase in the weight of the parotid glands compared to the controls (p<0.01). On the other hand, the total protein and α-amylase levels of the glands increased significantly by the drugs (p<0.01). SDS-PAGE of the parotid glands revealed new protein bands in the dobutamine and terbutaline groups. The density of the protein bands with molecular weights of about 50 and 40 Kd in the experimental groups showed that the synthesis and storage of amylase increased in the parotid glands by long-term administration of the drugs. A 37 and 21 Kd increase in the density of the protein bands in the dobutamine and terbutaline groups shows that the synthesis of proline-rich proteins (PRPs) may have increased. Also, this research indicates that the number of β-adrenoceptors may be high in the mouse parotid gland.

 



Volume 2, Issue 2 (11-1998)
Abstract

  In this study, the effects of lead acetate on two types of pain (nociception and inflammation) induced by formalin and its interaction with the opioid system and morphine-induced analgesia were examined. Male albino mice weighing 22-27 g were used in the experiments. Morphine was administered subcutaneously 30 minutes before formalin injection. Lead acetate was intraperitoneally administered 90 minutes before any injection. Different doses of morphine induce antinociception in both phases of the formalin test. Lead acetate induced no does-dependent nociception in the early phase, but caused dose-dependent analgesia in the late phase. Pretreatment with lead acetate antagonized the effect of morphine in the early phase. On the other hand, the effect of lead acetate in the early phase was reduced by morphine and its effect was eliminated in the late phase. We conclude that lead acetate can modulate the pain response and interact with morphine-induced antinociception. Additional research is suggested to identify the mechanisms of these effects.

 



Volume 3, Issue 1 (4-1999)
Abstract

  In this study interaction of three types of calcium channel blockers nifedipine, diltiazem and verapamil on the effects of lead acetate on two types of pain (nociception and inflammation) induced by formalin in mice were examined. In order to study nociception, formalin test was selected because of greater resemblance to clinical pain. Lead acetate (50, 75, l00, 125 and 150 mg/kg) administered intraperitoneally 90 minutes before formalin injection. Nifedipine (5 mg/kg), diltiazem (10 mg/kg) and verapamil (5 mg/kg) alone or in combination with different doses of lead acetate were used. Different doses of lead acetate induced a dose-dependent anti- nociception in both phases of formalin test. When animals were administered alone by calcium channel blockers, among them diltiazem and verapamil did not induce any significant effect in both phases of formalin test but nifedipine induced anti-inflammatory effect in late phase significantly (p<0.01). Pretreatment of animals with nifedipine and verapamil potentiated lead acetate anti-nociceptive effect (early phase) in doses of 50, 75 and 50 mg/kg, respectively. Both nifedipine and diltiazem augmented lead acetate anti-inflammatory effects (late phase) in all doses used. Pretreatment of animals with verapamil did not affect lead acetate anti-nociceptive or anti-inflammatory effects. Based on these data, tile association between calcium channel blockers and lead may be explained as a synergistic action rather than a simple dose combination of both agents. It is concluded that L-type calcium channels are susceptible to lead acetate that may be blocked during lead poisoning but different L-type calcium channel subtypes have different sensitivity to lead neurotoxicity.



Volume 3, Issue 1 (4-1999)
Abstract

  Bibliographical studies have been done on plants that are used as analgesics in traditional medicine, and Mellissa officinalis or Lemon Balm (LB) that there are some evidence indicating for its application as analgesics or its probable analgesic effect was selected for evaluation of analgesic effect by tail-flick test in mice. After scientific identification, the leaves and flowered branches of LB were used for extraction by two methods, perculation and suxhelet. Male Albino mice, weighing 20-30 grams and aging 4-6 weeks, were utilized in 9-inserted groups. Methanolic perculated extract of LB with different doses 50, 75, 100, 200 and 300 mg/kg were injected intraperitoneally to experimental animals. Suxhelet extract was injected with a dose of 200 mg/kg. Aspirin 300 mg/kg and morphine 2.5 mg/kg were injected into the positive control groups and normal saline 10 ml/kg was injected into the negative control groups. The analgesic effect of the plant extracts and the drugs was measured for 120 in periods of 15, 30, 45, 60, 90 and 120 minutes after injection. The results show that LB extract has analgesic effect and the most analgesic effect was induced by 200 mg/kg of extract 15 minutes after injection. However, perculation extract has more analgesic effect than suxhelet extract. There are no significant differences between the analgesic effect of LB extract with morphine 2.5 mg/kg in the 15, 90 and 120 min and ASA 300 mg/kg in the 15, 60 and 90 min after injection.


Mohammad Reza Zarrindas, Farzaneh Samiie, Ali Akbar Haeri Roohani, Seyed Mahdi Rezayat,
Volume 3, Issue 2 (11-1999)
Abstract

In the present study the effect of intracerebroventricular (ICV) injection of cerulein, an agonist of CCK receptor and proglumide, a receptor antagonist for hyperalgesia induced by sciatic nerve ligation were investigated in mice. Subcutaneous administration of morphine caused anti-nociception in both intact and nerve-ligated mice. However, the response to opioids was lower in ligated mice as compared to the intact animals. Cerulein induced antinociception only in the nerve-Iigated animals. Combination of cerulein with morphine elicited higher response in both intact and ligated animals. However, the induced response was much prominent in ligated animals. Proglumide alone did not elicit any response in both groups. The antagonist decreased the response of cerulein in the non-ligated mice. In addition a low dose of proglumide in combination with cerulein induced antinociception in the ligated mice. It can be concluded that CCK receptor-related
Sadegh Valizadeh, Mohammad Reza Zarrindast,
Volume 4, Issue 1 (4-2000)
Abstract

This study was designed to investigate the role of GABAB receptor agents on imipramine-induced antinociception in ligated and non-ligated mice using hot-plate test. The data showed that different doses of morphine (3, 6, and 9 mg/kg) induced a dose-dependent antinociception in ligated and non-ligated mice. However, the opioid response was decreased in ligated animals. Intracerebroventricular (i.c.v.) administration of imipramine (5, 10, 20, and 40 µg/mouse) did not induce antinociception in either non-ligated or ligated mice. However, the induced response in the ligated mice was less than that induced in the non-ligated mice. Intraperitoneal (i.p.) administration of imipramine (10, 20, 30, and 40 mg/kg) induced antinociception in both ligated and non-ligated mice. The responses to the drug were not significantly different in the two groups. Administration of baclofen either i.c.v. (0.125, 0.25, and 0.5 µg/mouse) or i.p. (0.5, 1,2, and 4 mg/kg) induced antinociception. The response to the drug was not significantly different in ligated and non-ligated mice. Intracerebroventricular administration of a lower dose of baclofen (0.125 µg/mouse) with different doses of imipramine (2.5, 5, and 10 mg/kg) potentiated the response to imipramine. This effect was reduced by i.c.v. injection of GABAB receptor antagonist, CGP35348 [P-(3-aminopropyl)-p-diethoxymethyl- phosphinic acid] at a dose of 20 µg/mouse. The higher dose of antagonist (20 µg /mouse) also decreased the response induced by baclofen or imipramine. CGP35348 itself (2.5, 5, 10, and 20 µg/mouse) induced a dose-dependent antinociception with no significant difference in the ligated and non-ligated mice. It is concluded that a GABA receptor mechanism(s) may modulate the antidepressant-induced antinociception.
Valiolah Hajhashemi, Taghi Ghafghazi, Mohammad Reza Nikravan,
Volume 6, Issue 1 (4-2002)
Abstract

Recent studies have shown that NMDA receptors are involved in the tolerance and dependence to opioids. In addition, it has been reported that ketamine, dextromethorphan and amantadine have antagonistic activity at NMDA receptors. Therefore, this study was conducted to clarify the effect of these drugs on morphine withdrawal syndrome. Morphine dependence was induced by increasing doses of morphine (30, 45, 60, and 90 mg/kg, s.c.) administered at 2 h intervals. Dextromethorphan (12.5, 25, and 50 mg/kg), amantadine (50, 100, and 150 mg/kg), ketamine (50 mg/kg), and clonidine (0.2 mg/kg) were injected (i.p.) 90 minutes after the last injection of morphine. Furthermore, these drugs were administered orally 60 minutes after the last morphine injection. All animals received naloxone (5 mg/kg, i.p.) 2 h after the last morphine injection. Withdrawal syndrome (number of jumping, standing on feet. and diarrhea) was recorded during a 30-min period. Dextromethorphan and amantadine inhibited jumping, standing on feet and diarrhea in a dose-dependent manner. Ketamine (50 mg/kg) had a similar effect and clonidine produced an almost complete inhibition of withdrawal syndrome. Although these test drugs belong to different pharmacological classes, but they share NMDA receptor antagonistic effect and it may be the probable cause for inhibition of withdrawal syndrome.

Volume 9, Issue 2 (11-2005)
Abstract



Volume 9, Issue 2 (11-2005)
Abstract



Volume 10, Issue 0 (9-2006)
Abstract


Ali Akbar Aliabadi, Hedayat Sahraei, Mehrangiz Sadooghi, Hasan Ghoshooni, Mehrvaz Alaf-Javadi, Seyed Hasan Salimi, Amir Abbas Barzegari,
Volume 10, Issue 1 (4-2006)
Abstract

Introduction: The influence of ascorbic acid on the nicotine-induced conditioned place preference (CPP) and behavioral sensitization was investigated in the present study. Methods: In a pilot study, place conditioning and locomotor activity were investigated after nicotine (0.25, 0.5, 0.75, 1, 1.5 and 2 mg/kg) or ascorbic acid (1, 10, 100 and 1000 mg/kg) administration. Different doses of ascorbic acid in conditioning days or on the test days were used. Behavioral sensitization was induced in animals by daily intraperitoneal administration of nicotine (0.25 mg/kg) for seven cosecutive days followed by one day interval. On 9th day, locomotor activity was induced by ineffective dose of nicotine (0.1 mg/kg). Ascorbic acid was injected 20 min before each injection of nicotine (acquisition of sensitization) or acutely 20 min before a challenge nicotine injection (expression of sensitization). Results: The results showed that intraperitoneal nicotine (1 mg/kg) administration can induce place preference whereas acute administration of the drug induces catalepsy. Administration of ascorbic acid did not induce place preference nor place aversion and also did not change the locomotor activity. Locomotor sensitization in mice was produced by intraperitoneal injection of nicotine (0.25 mg/kg) for 7 consecutive days. On the 9th day of experiments, activity of the mice was recorded after challenge with nicotine (0.1 mg/kg, i.p.). The senisitization was better achived when the ineffective dose of nicotine (0.1 mg/kg) was applied. Administration with ascorbic acid reduced both the acquisition and expression of nicotine-induced CPP. It was shown that ascorbic acid attenuated the acquisition of nicotine sensitization in a dose-independent manner but the expression of nicotineinduced sensitization was not affected by ascorbic acid. Conclusion: We conclude that ascorbic acid may interfere with nicotine-induced place preference and behavioral sensitization.
Parivash Hafez-Amini, Jamal Shams, Ali Shabahng-Saber-Tehrani, Ali Haeri-Rohani, Kazem Parivar, Vahab Babapour, Hedayat Sahraei,
Volume 10, Issue 2 (3-2006)
Abstract

Introduction: Several investigations have indicated that dopamine D receptors could influence morphine 2 eward. The influence of olanzapine (a D dopamine receptor antagonist) on the morphine-induced conditioned 2 lace preference (CPP) in male and female mice was investigated in the present study. Methods: The effects of olanzapine on the acquisition and expression of morphine CPP in male and female -MRI mice (W: 20-25 g) were investigated in the present study. Resultd: Subcutaneous (s.c.) injection of morphine (1-10 mg/kg, three drug sessions) induced place preference oth in male and female mice. Intraperitoneal (i.p.) administration of olanzapine (0.5-5 mg/kg) induced place version (CPA) in female mice but not in male mice. Administration of olanzapine (1, 2.5, 5 mg/kg, i.p.) reduced oth the acquisition and expression of morphine-induced CPP in male and female mice. However, olanzapine (5 g/kg, i.p.) caused more than 80% mortality in female but not male mice. The effects of olanzapine were reversed y L-arginine (20 mg/kg, i.p.) pre-administration. Conlusion: We conclude that olanzapine reduced morphine effects via different mechanism/s.
Mohammad Kazem Gharibnaseri, Seyed Ali Mard,
Volume 10, Issue 4 (1-2007)
Abstract

Introduction: Alhagi camelorum belongs to the Leguminosae family is used in Iranian folk medicine to treat some gastric diseases. The present study was undertaken to evaluate the Alhagi camelorum aqueous extract for anti-ulcer activity in rats. Methods: Male Wistar rats were pretreated with the A. camelorum aqueous extract (150, 300 or 450 mg/kg of B.W., P.O.) before induction of gastric ulcer by water immersion restraint-stress at 20-22 °C (5 h) or before induction of the ulcer by ethanol 100% (1 ml/200g of B.W., P.O.). Negative control animals received saline (0.5 ml/100 g of B.W.). Positive control animals received ranitidine (60 mg/kg, P.O.). Results: The A. camelorum aqueous extract (ACE) protected rats against water immersion restraint-stress and ethanol-induced ulcers in a dose-dependent manner. In water immersion restraint induced ulcerated rat, the ACE increased pH and reduced gastric acid content. ACE did not show any signs of toxicity and mortality up to10 g/kg, P.O. in mice. Conclusion: The results suggest that A. camelorum aqueous extract can exert significant mucosal protection and antisecretory effects on gastric mucosa in rats.
Fatemeh Farokhi, Seyed Said Pournaghash Tehrani, Hedayat Sahraei, Azam Bakhtiarian, Hassan Ghoshooni, Seyedeh Maedeh Fatemi, Jamal Shams,
Volume 11, Issue 1 (4-2007)
Abstract

Introduction: Topiramate is a newly anti-convulsant drug, which acts as NMDA glutamate receptor antagonist as well as the GABAB receptor agonist. It is used for physical dependence to opioids as well as cocaine, nicotine, alcohol and ecstasy dependence. In the present study attempts were made to further identification of the effects of topiramate on the acquisition and expression of morphine-induced conditioned place preference and behavioural sensitisation in mice. Methods: Male Swiss-Webster mice were used. Conditioned place preference and locomotion were assessed by an un-biased place conditioning paradigm and open filed methods. In a pilot study, the effects of morphine and topiramate on place conditioning paradigm as well as locomotion were assessed in morphine-nave animals for evaluation of effective and ineffective doses of the drugs. Different doses of topiramate were injected to the animals 30 min before each morphine injections (acquisition) or 30 min before the experiments were beginning on the test day. Results: Administration of different doses of morphine (0.5, 5 and 50 mg/kg) induced locomotor activity in the animals. In addition, morphine (1, 10 and 20 mg/kg) administration also induced place preference. On the other hand, administration of different doses of topiramate (20, 80 and 120 mg/kg) neither induced place preference nor altered animals’ activity. Topiramate administration (20 and 80 mg/kg) and (80 and 120 mg/kg) reduced the acquisition and expression of morphine-induced place preference, respectively. In addition, topiramate (20, 80 and 120 mg/kg) reduced the acquisition of morphine-induced behavioral sensitization where as the drug in dose 80 mg/kg enhanced the expression of morphine-induced behavioral sensitization. Conclusion: It can be concluded that topirmate administration interacts with the euphoric and locomotor properties of morphine and this can be considered in therapeutic usage of the drug.

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