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Showing 9 results for Asgari

Mohsen Foadodini, Hasan Firooz-Abadi, Ali Khosh Baten, Alireza Asgari, Hedayat Sahraei, Hasan Ghoshooni,
Volume 2, Issue 1 (Spring and Summer 1998)

  The involvement of nitric oxide (NO) in the reinforcing properties of opiate reward was studied by examining the effect of a NO precursor (L-arginine) and a NO synthase inhibitor (L-NAME) on the rate of intravenous self-administration of morphine. This experiment was investigated in male albino Sprague Dawley rats (300 ± 50 g). At doses of 5 and 10 mg/kg (i.p.), L-arginine decreased morphine self- administration significantly, while 20 and 60 mg/kg doses were not significantly effective. In addition, L-arginine per se induced self-administration behavior. At doses of 0.75, 1.25, 2.5, and 5 mg/kg (i.p.), L-NAME had no effect on self-administration, whereas injection of 5 mg/kg 60 minutes before the test did increase self-administration significantly. We may therefore conclude that NO is involved in the VTA-mesolimbic pathway, and it can be involved in the psychological dependence to morphine.

Hedayat Sahrai, Mohammad Reza Shariati, Hasan Aghai-Firoozabadi, Ali Khoshbaten, Alireza Asgari, Hasan Ghoshooni,,
Volume 2, Issue 2 (Fall and Winter 1998)

  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.


Hedayat Sahraie, Hasan Ghoshooni, Gila Pirzadeh Jahromi, Ali Reza Asgari, Gholamreza Pourheydari, Ali Khoshbaten,
Volume 7, Issue 1 (Spring and Summer 2003)

It has been shown that L-arginine like the abused drugs could release dopamine from meso-cortico-limbic system. The purpose of the present study was to compare the effect of L-arginine with morphine as a standard abuse drug in the induction of conditioned place preference (CPP) in rat. For this purpose, male Wistar rats (250-300 g) were used in the experiments. Five days after surgical cannulation in the ventral tegmental area (VTA), different doses of L-arginine, L-NAME or morphine were injected and conditioned biased method was preformed. The results showed that: 1. Intraperitoneal (i.p.) (0.1, 1 and 5 mg/kg) but not intra-VTA (i-VTA) (0.3, 0.1 and 3 µg/rat) injections of L-arginine induced CPP in a dose-dependent manner. Injection of 10 mg/kg (i.p.) and 2 µg/rat of morphine (i-VTA) also caused a significant CPP in rats. Both i.p. (0.1, 1 and 5 mg/kg) and i-VTA (0.3, 0.1 and µg/rat) injection of L-NAME did not produce any effect in the rats, but the drug at higher dose (5 mg/kg, i.p.) attenuated the CPP induced by L-arginine (5 mg/kg, i.p.) Administration of morphine (10 mg/kg, i.p.) on three consecutive days and, then with 3-day interval caused the occurrence of sensitization to morphine, so that injection of ineffective dose of morphine (0.5 mg/kg, i.p.) induced CPP in sensitized rats. However, when the procedure was repeated for L-arginine (5 mg/kg, i.p.), rats showed negative response to the ineffective dose of L-arginine (0.1 mg/kg, i.p.). Meanwhile, in rats that received L-arginine (5 mg/kg, i.p.) on training days, injection of the same dose L-arginine on the test day dramatically decreased the time spent in drug-paired side while injection of morphine (10 mg/kg, i.p.) on the test day to those rats which had received morphine (10 mg/kg, i.p.) on training days caused an increase in time spent in the drug-paired compartment. It could be concluded that i.p. injection of L-arginine causes significant CPP rats and this behavior was attenuated by nitric oxide synthase inhibitor, L-NAME. Furthermore, the site of action of the drug seems not to be VTA. On the other hand behaviors due to administration of L-arginine did not show some properties of abused drugs such as sensitization and state dependency.
Jafar Vatanparast, Mahyar Janahmadi, Houri Sepehri, Ali Haeri-Rohani, Ali Reza Asgari,
Volume 10, Issue 1 (Spring 2006)

Introduction: Since organophosphorus compounds (OP) are toxic and designed to destroy insects and pest species, there are many hazards associated with their use. Although, the main target site of these compounds is acetylcholinesterase (AChE), however it has become increasingly evident that OPs have also other direct effects on cellular processes. In the present study, the effects of low concentrations of paraoxon and its interaction with forskolin, an activator of protein kinase A (PKA), were studied on Ca2+ spike configuration and frequency in neurons of snail Caucasotachea atrolabiata. Methods: Subesophageal ganglia neurons were recorded in current clamp mode in Na+ free Ringer solution that contained voltage dependent potassium channel blockers, 4AP and TEA. Results: Paraoxon (0.3-0.6 μM) decreased the duration of spontaneous Ca2+ spikes. This effect was seen with a suppression of single spike AHPs, leading to an increment in firing rate. Paraoxon induced hyperactivity appeared to be a consequence of decrease in Ca2+ influx during spikes which is the main determinant of AHP duration by activating Ca2+ dependent potassium channels. Forskolin (25 μM), in the absence of a significant change in spike duration, decreased the duration of single spike AHPs and increased the frequency of spikes. After forskolin application, paraoxon decreased the duration of Ca2+ spikes and AHPs, and increased the activity. However, these effects, especially on spike duration, were not as pronounced as in the absence of forskolin. Conclusion: These findings suggest that although forskolin, similar to paraoxon, decreases the AHP and increases the frequency of spikes but it employs mechanism(s) different from paraoxon which also oppose the effects of paraoxon on Ca2+ spikes configuration and frequency.
Ameneh Shahroukhi, Asghar Qassemi, Fereshteh Pourabdolhossein, Ali Khoshbaten, Alireza Asgari,
Volume 10, Issue 3 (Fall 2006)

Introduction: Compounds which are used to treat organophosphate (OP) poisoning are not able to fully alleviate long lasting effects. They are mainly used to antagonize cholinergic effects of Ops. However, non-cholinergic effects, such as interference with different neurotransmitter systems, especially GABA release and uptake, are recently attracting more attentions. We have tried to investigate any potential interaction between paraoxon and GABA uptake. Methods: We used cerebellar synaptosomes. Cerebellum of 250-280 g Wistar rats were rapidly dissected out, homogenized, centrifuged, and incubated with 0.01 μ M [3H]GABA in the presence of different doses of paraoxon for 10 minutes at 37 oC. At the end of the incubation period, synaptosomes were layered in chambers of superfusion system. In order to assay the amounts of [3H]GABA taken up, radioactivity was measured using a β-counter. Results: Our findings reveal that mean GABA uptake was 111.42, 95.37, 71.6, 73.53 and 75 percent of the control values in the presence of different concentrations of paraoxon (0.01, 0.1, 1, 10 and 100μ M) respectively. GABA uptake was significantly reduced at doses 1, 10 and 100μ M (p<0.05). Conclusion: It seems that paraoxon at higher doses may interfere with GABA uptake by cerebellar synaptosomes.
Moslem Mohammadi, Asghar Ghasemi, Esmaeel Ghani, Ali Khoshbaten, Alireza Asgari,
Volume 13, Issue 2 (Summer 2009)

Introduction: Paraoxon (the neurotoxic metabolite of organophosphorus (OP) insecticide, parathion) exerts acute toxicity by inhibition of acetylcholinesterase (AChE), leading to the accumulation of acetylcholine in cholinergic synapses and hence overstimulation of the cholinergic system. Since, reports on changes in the level of γ- amino butyric acid (GABA) during OP-induced convulsion have been controversial, in present study we used cortical and hippocampal synaptosomes from rats after paraoxon poisoning to detect changes in GABA uptake. Methods: Male Wistar rats (200-270 g) were used in this study. Animals were given a single intraperitoneal injection of corn oil (vehicle group) or one of doses of paraoxon (0.1, 0.3, or 0.7 mg/kg) and [3H]GABA uptake by cerebral cortex and hippocampal synaptosomes was measured at 30 min, 4 h, and 18 h after the exposure (n= 7 rats/group). Type of transporter involved in the uptake was also determined using β-alnine, and L-diaminobutyric acid (L-DABA), a glial and a neuronal GABA uptake inhibitor, respectively. Results: GABA uptake was significantly (p<0.001) reduced by both cerebral cortex (18-32%) and hippocampal (16-21%) synaptosomes compared with their respective control groups at all three time points after administering 0.7 of paraoxon (convulsive dose). β-alnine had no inhibitory effect on the uptake, whereas L-DABA abolished most of the transporter mediated GABA uptake. Conclusion: Since GABA uptake did not change in other two paraoxon treated groups, it may be indicating that decrement of GABA uptake is convulsion-related. The decrease in GABA uptake, presumably due to a change in the function of GABA transporters, may represent a compensatory response modulating neuronal overexcitation. Most of synaptosomal GABA uptake was blocked by L-DABA, indicating that the uptake was primarily by a neuronal GABA transporter (GAT), GAT-1.
Mohammad Reza Naghii, Mahmood Mofid, Ali Reza Asgari, Mahdi Hedayati, Maryam Sadat Daneshpour,
Volume 15, Issue 3 (Fall 2011)

Introduction: Boron possesses widespread properties and is important for human and animal nutrition. Since Boron is rapidly bioavailable, the objective of the present study was to determine whether acute (hourly or daily), and weekly supplementationcould have any significant biological effects on the synthesis of steroids as well as inflammatory biomarkers. Methods: Eight male volunteers participated in experiments on three occasions (day 0, 1 and 7). On the first day (day 0), a blood sample was collected at 8.00 A. M, followed by ingestion of placebo. On the next day (supplementation- day 1), similar procedure was followed by ingestion of 10 mg of boron capsule. On both occasions samples of blood were collected every 2h for the next 6 h. Subjects consumed a capsule of 10 mg boron every day and on day 7, blood collection was carried out again at 8.00 A.M. Independent sample t-tests were used to evaluate the differences. Results: Plasma boron was significantly increasedfollowing hourly (P=0.002) and weekly (P=0.000) consumption of boron. After one week of supplementation, free testosterone levels were significantly increased (P<= 0.02) and estradiol concentrations were significantly decreased (P<= 0.01). Dihydrotestosterone (DHT), cortisol and Vitamin D showed slight non significant, increases. The ratios of free testosterone/testosterone (FT/T) (P<= 0.001), free testosterone/estradiol (FT/E2) (P<= 0.004) and testosterone/estradiol (T/E2) (P<= 0.009) were significantly increased. Also, all 3 inflammatory biomarkers were decreased after supplementation. Conclusion: Although there are previous studies that report a decrease in proinflammatory cytokines induced by boron consumption, to our knowledge, this is the first human study reporting an increase in plasma free testosterone concentrations following consumption of a boron supplement. This indicates a possible protective role against diseases of pathological conditions for this microelement.
Mostafa Rahimi, Ali Reza Asgari, Ali Khoshbaten,
Volume 18, Issue 2 ( Summer 2014)

Cardiovascular diseases are still the main cause of mortality around the world. Therefore, it is essential to develop practical means to reduce their burden. A wealth of evidence supports the role of physical exercise in attenuating many of the risk factors of cardiovascular diseases. Moreover, endurance training warrants protection against myocardial infarction. Exercise, even if performed only in a few days, can protect the heart against ischemia-reperfusion (IR) injury, and this protection will be even more in longer exercises. It is yet to be clarified how exercise maneuvers provide protection against IR. However, it is suggested that some molecular and cellular mechanisms in addition to metabolic and hormonal alterations are seemingly involved in exercise-induced cardioprotection (EICP), such as increased capacity of antioxidant system, higher expression of heat shock proteins, improvement in ATP-sensitive potassium channels, change in nitric oxide production, and adaptive cardiac mitochondrial modulations. This paper discusses the current data on molecular and cellular mechanisms of EICP. Understanding the molecular basis of EICP against IR injury will provide us with the required knowledge for development of preventive and therapeutic approaches. In addition, exercise characteristics leading to more pronounced cardioprotection will be concisely addressed.
Sahand Asharfpour, Fereshteh Pourabdolhossein, Forough Ebrahim Tabar, Manouchehr Ashrafpour, Mojdeh Navidhamidi, Sima Shahabi, Maryam Ghasemi-Kasman, Alireza Asgari,
Volume 22, Issue 2 (June 2018)

Introduction: Synaptosomes are sealed particles that contain mitochondria, cytoskeleton and vesicles which are necessary to synaptic events like neurotransmitter release and uptake in the nervous system. However, the effect of high and low temperatures on synaptosome membrane integrity and function during a time course after its extraction is less known. The purpose of this study was to assess synaptosome viability and function at 37, 4°C and room temperature (RT) during 6 hours after its extraction. Methods: Hippocampi of 40 male Wistar rats were used for synaptosome preparation. To ensure synaptosome membrane integrity and function, lactate dehydrogenase activity (LDH) and GABA uptake were assessed during 6 successive hours after their extraction at 37, 4°C and RT. Results: Our results showed that at 37°C, synaptosome membrane integrity was reduced 3 hours but at 4°C and RT, it occurred 5 hours following their extraction. The results of synaptosome function analysis coincide with LDH enzyme assay data, meaning that GABA uptake faced a 50% reduction from the initial value at 37°C after 3 hours and at RT after 5 hours. We also found that GABA uptake was reduced at 4°C in the first hour after extraction because the low temperature inhibits GABA transporters. Conclusion: Synaptosomes preserved their viability and function at RT, 37 and 4°C at least for 3 hours after extraction and reduced over time. For long term application of synaptosomes, it is better to keep them at 4°C.

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