new approach for aggregation of Paramecium caudatum by nitric oxide

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. 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. Morphine, particularly 0.5 to 60 microg/microl, aggregated the Paramecia. The infusion of L-arginine [1 to 8 microg/microl] together with morphine potentiated this effect, though, pre-usage of L-NAME [1 to 8 microg/microl], 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. This study introduces a new approach to involve NO in physiology of aggregation of Paramecia following exposure to the misused sedative drug, morphine

Nitric oxide-induced polycystic ovaries in the wistar rat

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. 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. 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. Based on these results, we believe that NO may play a major role in the pathophysiology of PCOS

Blockade of the naloxone-induced aversion in morphine-conditioned wistar rats by L-arginine intra-central amygdale

Single injection of naloxone, a selective antagonist of morphine, prior to the drug conditioning testing was used to investigate on morphine dependence. 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 amygdale prior to naloxone-paired place conditioning testing. 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 micro g/rat, intra-central amygdale] prior to naloxone on the day of the testing. The response to L-arginine was blocked by pre-injection of N[G]-nitro-L-arginine methyl ester [L-NAME] intra-central amygdale]. 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 amygdale most likely plays a key role in this phenomenon

Reversal effect of intra-central henobar microinjection of L-arginine on place aversion induced by naloxone in morphine conditioned rats

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. 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 henobar [CeA] prior to naloxone injection pre-testing. 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 micro g/rat], intra-CeA prior to naloxone administration. However, pre-injection of L-NAME [intra-CeA], an inhibitor of NO production, blocked this effect. The finding may reflect that NO in the nucleus participates in morphine plus naloxone interaction

Verifying of participation of nitric oxide in morphine place conditioning in the rat medial septum using nicotinamide adenine dinucleotide phosphate-diaphorase [NADPH-d]

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. Effects of intraseptal injections of L-arginine and/or N[G]-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. Morphine induced a significant CPP in the rats. Single injections of L-arginine or L-NAME [0.3, 1.0 and 3.0 micro g/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 micro g/rat] did not affect morphine response. However, administration of L-arginine [0.3, 1.0 and 3.0 micro g/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 micro g/rat] to L-arginine [0.3 micro g/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. 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