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Introduction: Morphine induces ovarian cysts that cause obesity and disrupt sex hormone secretion. Baclofen, a gamma-aminobutyric acid receptor agonist, can help regulate sex hormones and reduce harmful blood lipids by protecting against morphine-induced gamma-aminobutyric acid inhibition. We investigated the prophylactic effect of baclofen in rats receiving morphine by comparing with the untreated groups. Materials and Methods: Forty eight female Wistar rats were randomly divided into several groups, including control (saline 1 mL/kg, i.p.), morphine (5 mg/kg, i.p.), baclofen (10, 20, and 30 mg/kg, i.p.), and baclofen (10, 20, and 30 mg/kg) before morphine (5 mg/kg). Twenty four hours after the treatment, blood and serum samples were taken to check the levels of gonadotropins (LH & FSH) and lipid profile. The ovaries and uterus were also studied, and a proinflammatory nitric oxide (NO) diagnostic test was completed. The results were analyzed using analysis of variance (α = 0.05). Results: In comparison with the control group, the levels of LH and not FSH decreased in the morphine group and the number of ovarian cysts was more in the morphine group. These problems were not observed in the group of baclofen alone and baclofen + morphine. However, the triglyceride level increased slightly in the baclofen 30 mg/kg + morphine group. But the LDL level somewhat decreased. The proinflammatory NO system did not show significant activation in the ovary and uterus, except for the baclofen 10 mg/kg + baclofen group. Conclusion: Morphine can cause ovarian cysts by lowering LH but baclofen prophylaxis can protect reproductive properties by adapting major metabolic changes. [ABSTRACT FROM AUTHOR]

Byline: Manizheh. Karami, Samira. Geravand, Mahnaz. Rahimpour Background and Objective: Aluminum chloride (AlCl3) can impair spatial memory recovery. We investigated the protective effect of L-arginine, a precursor of nitric oxide [...]

Byline: Manizheh. Karami, Mahnaz. Rahimpour, Sara. Karimi, Hedayat. Sahraei Objective: The aim of this study was to evaluate if nitric oxide (NO) in the central amygdala (CeA) is involved in [...]

Byline: Manizheh. Karami, Nosaibeh. Riahi, Mohammad. Nadoushan Objective: Colchicine, a potent neurotoxin derived of plant has been recently identified as a degenerative toxin of small pyramidal cells in the hippocampal [...]

Byline: Masoomeh. Biglarnia, Manizheh. Karami, Zahra. Hafshejani Objective: Antinociceptive effect of morphine in offspring born of mothers that received saline or morphine during the gestation period was investigated. Materials and [...]

Byline: Zahra. Hafeshjani, Manizheh. Karami, Masoomeh. Biglarnia Objective: Role of nitric oxide (NO) in reversing morphine anti-nociception has been shown. However, the interaction between NO and naloxone-induced pain in the [...]

Objective(s): With no substantial cost, we injected L-arginine into the rat’s corpus callosum (CC) to create animal model of multiple sclerosis (MS) and investigated the pre-injection effect of gold nanoparticles (GNPs). Materials and Methods: Adult male Wistar rat (250-300 g) was surgically cannulated at the CC, and after recovery it was injected L-arginine (3-200 μg/rat, intra-CC) once daily for 3 to 5 consecutive days. GNPs (0.001-0.01 μg/rat, intra-CC) were injected alone or prior to the L-arginine using the same procedure. Control group solely received saline (1 μL/rat, intra-CC). Brain was studied with luxol fast blue. Weight change was also analyzed via the analysis of variance (ANOVA). Results: L-arginine significantly induced (p< 0.05) a reduction in the fiber density while the neurons increased (p< 0.05). Single GNPs reduced (p< 0.05) the fiber and neuron densities; however, pre-injection of NPs caused myelinated fibers and uniform density of neurons. Conclusion: The L-arginine may trigger demyelination by pro-inflammatory nitric oxide (NO), and the GNPs may improve this effect. [ABSTRACT FROM AUTHOR]

Colchicine, a potent neurotoxin derived from plants, has been recently introduced as a degenerative toxin of small pyramidal cells in the cortical area 1 of the hippocampus (CA1). In this study, the effect of the alkaloid in CA1 on the behaviors in the conditioning task was measured. Injections of colchicine (1,5 µg/rat, intra-CA1) was performed in the male Wistar rats, while the animals were settled and cannulated in a stereotaxic apparatus. In the control group solely injection of saline (1 µl/rat, intra-CA1) was used. One week later, all the animals passed the saline conditioning task using a three-day schedule of an unbiased paradigm. They were administered saline (1 ml/kg, s.c.) twice a day throughout the conditioning phase. To evaluate the possible effects of cell injury by the toxin on the pyramidal cells, both the motivational signals while in the conditioning box and the non-motivational locomotive signs of the treated and control rats were measured. Based on the present study the alkaloid caused no change in the score of place conditioning, but affected both the sniffing and grooming behaviors in the group that received colchicine. However, the alkaloid did not show the significant effect on the rearing or compartment entering in the rats. According to the findings, the intra-CA1 injection of colchicine may impair the neuronal transmission of non-motivational information by the pyramidal cells in the dorsal hippocampus. [ABSTRACT FROM AUTHOR]

Background and Objective: Nitric oxide (NO) plays a role in thermoregulation and growth of protozoa. This work aimed to add the molecule NO in physiology of protozoa in contact with abused narcotic substances. Materials and Methods: A sedative drug, morphine, was infused into a cell chamber containing Paramecia. The cell response to the drug was recorded promptly after drug infusion using a potency protocol provided for the first time at this laboratory. A precursor of NO, L-arginine, was treated jointly with drug to involve the NO system in protozoan performance to drug exposure. Marking of NADPH-diaphorase (NADPH-d) was followed to provide data to explain the mechanisms. Results: Morphine, particularly 0.5 to 60 µg/µl, aggregated the Paramecia. The infusion of L-arginine (1 to 8 µg/µl) together with morphine potentiated this effect, though, pre-usage of L-NAME (1 to 8 µg/µl), a blocker of NO production, reversed the response. Notably the activation of NADPH-d in solely morphine or L-arginine plus morphine samples was revealed. However, the expression of marker was attenuated upon pre-infusion with L-NAME. Conclusion: This study introduces a new approach to involve NO in physiology of aggregation of Paramecia following exposure to the misused sedative drug, morphine. [ABSTRACT FROM AUTHOR]

Downward phase of dose-response morphine converted U shape curve was chosen as a base for investigating the effects of different doses of naloxone (0.05-0.4 mg/Kg) on morphine reward/aversion properties using place preference method. First, male Wistar rats (200-220 g) were received morphine (1-7.5 mg/Kg) for place conditioning and marginal dose of morphine (5 mg/Kg) calculated by GraphPad software. In the next part, the animals received different naloxone challenge doses (0.05-0.4 mg/Kg; IP) on the test day. Animals' behavior was monitored using a video camera during the test session. Time spent in each compartment was calculated as the main sign of drug seeking behavior. In addition, numbers of rearing and sniffing as well as locomotion activity for each animal were counted as important dopamine-dependent behavioral signs. More over, the total compartment crossing by each animal as the sign of decision making was also counted. Our results indicated that naloxone showed biphasic effects on the appearance of morphine-induced place preference. The antagonist potentiates the expression of morphine-induced place preference on the dose of 0.05 and 0.4 mg/Kg while inhibits the morphine effect on the dose of 0.1 mg/Kg. On the other hand, the total animal sniffing, rearing, locomotion, and compartment entering were not significantly changed among the groups. It could be concluded that the inhibition of opioid receptors may enhance or inhibit the expression of morphine reward according to the naloxone dose, which in turn indicate the influence of several opioid receptor in this regard. In addition, opioid receptor blocking did not enhance the signs of drug seeking behavior linked to the activity of mesolimbic dopamine system. [ABSTRACT FROM AUTHOR]

Objective(s) Single injection of naloxone, a selective antagonist of morphine, prior to the drug conditioning testing was used to investigate on morphine dependence. Materials and Methods Conditioning to morphine (2.5-10 mg/kg, s.c.) was established in adult male Wistar rats (weighing 200-250 g) using an unbiased procedure. Nitric oxide agents were microinjected into the central amygdala prior to naloxone-paired place conditioning testing. Results The results showed that morphine produced a significant dose-dependent place preference in animals. Naloxone (0.1-0.4 mg/kg, i.p.) injections pre-testing of the response to morphine (7.5 mg/kg, s.c.) caused a significant aversion at the higher doses (0.4 mg/kg, i.p.). This response was reversed by microinjection of L-arginine (0.3-3 μg/rat, intra-central amygdala) prior to naloxone on the day of the testing. The response to L-arginine was blocked by pre-injection of NG-nitro-L-arginine methyl ester (L-NAME) (intra-central amygdala). Conclusion A single injection of naloxone on the test day of morphine place conditioning may simply reveal the occurrence of morphine dependence in rats, and that the nitric oxide in the central amygdala most likely plays a key role in this phenomenon. [ABSTRACT FROM AUTHOR]

Colchicine, a potent neurotoxin derived from plants, has been recently introduced as a degenerative toxin of small pyramidal cells in the cortical area 1 of the hippocampus (CA1). In this study, the effect of the alkaloid in CA1 on the behaviors in the conditioning task was measured. Injections of colchicine (1,5 µg/rat, intra-CA1) was performed in the male Wistar rats, while the animals were settled and cannulated in a stereotaxic apparatus. In the control group solely injection of saline (1 µl/rat, intra-CA1) was used. One week later, all the animals passed the saline conditioning task using a three-day schedule of an unbiased paradigm. They were administered saline (1 ml/kg, s.c.) twice a day throughout the conditioning phase. To evaluate the possible effects of cell injury by the toxin on the pyramidal cells, both the motivational signals while in the conditioning box and the non-motivational locomotive signs of the treated and control rats were measured. Based on the present study the alkaloid caused no change in the score of place conditioning, but affected both the sniffing and grooming behaviors in the group that received colchicine. However, the alkaloid did not show the significant effect on the rearing or compartment entering in the rats. According to the findings, the intra-CA1 injection of colchicine may impair the neuronal transmission of non-motivational information by the pyramidal cells in the dorsal hippocampus.

Background: Nitric oxide (NO) involves in polycystic ovary syndrome (PCOS), a cause of infertility in women during the reproductive age. The PCOS is now categorized as an inflammatory phenomenon. The aim of this study was to evaluate the role of NO, a proinflammatory agent, in this syndrome at histological and biochemical levels., Materials and Methods: In this experimental study, animals were female Wistar rats (weighing 200-250 g) kept under standard conditions. L-Arginine (50-200 mg/kg), a precursor of NO, was injected intra-peritoneally (i.p.) through a period ranging from 9 to14 days/ once a day. The rats' estrous cycle was studied using Papanicolaou test; those showing phase of Diestrous were grouped into experimental and control groups. The control group solely received saline (1 ml/kg, i.p.) throughout all experiments. To evaluate the inflammatory effect of NO, the rats were treated an anti-inflammatory agent, naloxone hydrochloride (0.4 mg/kg, i.p.), prior to L-arginine. At the end of the treatment period all animals' ovaries were assessed for histopathological and histochemical investigations. Also, activation of NO synthase (NOS) in the experiments was studied using NADPH-diaphorase technique., Results: The ovaries of rats treated with L-arginine showed polycystic characteristics in contrast to those collected from control or naloxone pretreated groups, based on image analysis. A difference in enzyme activation was also shown in the sections that belonged to the groups that received L-arginine when compared with the pre-naloxone and control groups., Conclusion: Based on these results, we believe that NO may play a major role in the pathophysiology of PCOS.

This research was designed to study sexual differences in place conditioning induced by morphine in offspring born of female Wistar rats mated with drug-naïve males. Mothers were exposed to morphine during the 14(th)-16(th) days of gestational. Control dams were simply saline-injected. Female and male virgin offspring born of morphine-treated or saline-treated mothers were separately housed until become fully matured. A 3-day schedule of an unbiased conditioning procedure was used to the induce conditioning to morphine (2.5-7.5 mg/Kg, SC) in the offspring. According to the results, female offspring born of saline-administered mothers were morphine place-conditioned at lower doses of opioid (2.5 mg/Kg) in comparison to the males. An increase in locomotor activity in the females at 7.5 mg/Kg of opioid was also revealed. In contrast, administration of morphine (2.5-7.5 mg/Kg, SC), induced a significant aversion in either sexes of offspring born of morphine-exposed mothers. Moreover, female offspring of this category acquired more pronounced aversion at higher doses of morphine than males. In addition, a significant morphine-dose effect (7.5 mg/Kg, SC) on locomotor activity of these females' offspring was observed. This study may highlight sex differences in conditioning effects induced by morphine between offspring derived of morphine-treated mothers and those of saline-treated.

Background: Role of nitric oxide (NO) on expression of morphine conditioning using a solely classic task has been proposed previously. In this work, the involvement of NO on the expression of opioid-induced conditioning in the task paired with an injection of naloxone was investigated., Methods: Conditioning was established in adult male Wistar rats (weighing 200-250 g) using an unbiased procedure. Naloxone (0.05-0.4 mg/kg, i.p.), a selective antagonist of mu-opioid receptor, was administered once prior to morphine response testing. NO agents were administered directly into the central amygdala (CeA) prior to naloxone injection pre-testing., Results: Morphine (2.5-10 mg/kg, s.c.) produced a significant dose-dependent place preference in experimental animals. When naloxone (0.05-0.4 mg/kg, i.p.) was injected before testing of morphine (5 mg/kg, s.c.) response, the antagonist induced a significant aversion. This response was reversed due to injection of L-arginine (0.3-3 microg/rat), intra-CeA prior to naloxone administration. However, pre-injection of L-NAME (intra-CeA), an inhibitor of NO production, blocked this effect., Conclusion: The finding may reflect that NO in the nucleus participates in morphine plus naloxone interaction.

Background: Role of nitric oxide (NO) in morphine-induced conditioned place preference (CPP) has already been proposed in the rat medial septum (MS), but no molecular evidence has been provided to clear this fact., Methods: Effects of intraseptal injections of L-arginine and/or NG-nitro-L-arginine methyl ester (L-NAME) on morphine place conditioning in Wistar rats were examined. Morphine (2.5-7.5 mg/kg) was injected s.c. using a three-day schedule of an unbiased place preference. All of the brain samples were examined histochemically by nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d), the main marker for NO activation., Results: Morphine induced a significant CPP in the rats. Single injections of L-arginine or L-NAME (0.3, 1.0 and 3.0 µg/rat) did not induce CPP. In addition, co-administration of morphine (5.0 mg/kg) with L-arginine or L-NAME (0.3, 1.0 and 3.0 µg/rat) did not affect morphine response. However, administration of L-arginine (0.3, 1.0 and 3.0 µg/rat) prior to morphine conditioning testing enhanced the expression of morphine response. Moreover, pre-injection of L-NAME (0.3, 1.0 and 3.0 µg/rat) to L-arginine (0.3 µg/rat) did not reverse the response to the agent. The expression of NADPH-d was observed in the rat brain samples treated by L-arginine. A decreased expression of NADPH-d was also observed in rats pre-injected by L-NAME., Conclusion: This finding strongly suggests that NO system in the rat MS has an impact on the expression of morphine rewarding, and that the NO participates in place conditioning induced of morphine.