Nowadays, use of the nanoparticle materials especially Fe2O3 (Fe2O3 NPs) nanoparticles, are increased in deferent aspects such as medicine and agriculture. Previous studied are indicated that acute usage of Fe2O3 NPs could reduce memory in animal models. On the other hands, it is well known that central muscarinic cholinergic receptors are involved in memory formation process. In this research, involvement of cholinergic muscarinic receptors in CA1 region of dorsal hippocampus is studied in memory impairment induced by Fe2O3 NPs in adult male rat.
In this experimental research, 70 Wistar adult male rats were used. All animals were bilaterally implanted with cannulas into the CA1 and were trained in a step-through instrument for passive avoidance learning, after one week. Drugs (Fe2O3 NPs, pilocarpine, scopolamine and saline) were administrated immediately after training. Saline and Fe2O3 NPs injected as Intraperitoneal (ip). Saline, pilocarpine and scopolamine were injected as intra-CA1 region. Memory of the animals was evaluated by recording step-trough latency, 24 hours and seven days after training session.
Results indicated that injection of Fe2O3 NPs (7.5mg/kg, ip) decreased memory retrieval in passive avoidance memory in test day(p<0.01). Intra-CA1 microinjection of pilocarpine (1, 2 μg/rat), had no significant effects alone on memory retrieval, While, microinjection of pilocarpine (1, 2 μg/rat, intra-CA1) plus Fe2O3 NPs (7.5mg/kg), decreased the impairment effect of these nanoparticles on memory retrieval(p<0.05) ( p<0.01). Post training co-administration of ineffective doses of Fe2O3 NPs (5mg/kg, ip) and scopolamine (1µg/rat, intra-CA1) decreased the memory retrieval of animals in test day(p<0.01).
On the basis of the results of this research, it seems that Fe2O3 NPs probably is reduced memory impairment by decreases of the cholinergic muscarinic activity in CA1.

 

 

Anxiety is an adaptation response that is created in response to multiple physiological and environmental stresses and can protect a person against the risk. It is clear that involvement of various neurotransmitter systems have important role in the anxiety process, so far, several studies have been done in this field. Vitamin C (ascorbic acid) is a water-soluble antioxidant, which plays a role in many physiologic reactions in the body. On the other hand, nicotine has an anxiogenic effect. Opioid receptors play an important role in anxiety behaviors. The aim of this study was to investigate the interaction of vitamin C with opioid receptors on nicotine induced anxiety. Adult male mice were divided into 7 groups. Anxiety test was performed 30 minutes after intraperitoneal injection of drugs in an elevated plus maze apparatus. For this purpose, for 5 minutes, anxiety indices such as percentage of open arm entering (% OAE) and percentage of open arm time (% OAT) in the elevated plus maze system, and delay of the first head dipping and the number of head dipping in a Hole board apparatus was recorded. The results were analyzed by ANOVA and Tukey test. The results of this study showed that nicotine (0.8 mg/kg, ip) induced anxiety in animals. Vitamin C (80 mg/kg, ip) improved anxiogenic effect of nicotine. Naloxone (4mg/kg, ip) decreased the improvement effect of vitamin C (80mg/kg) on nicotine induced-anxiety. On the other hands, morphine (4mg/kg, ip) plus Vitamin C (40 mg/kg) increased this anxiolytic effect of vitamin C. Therefore, based on the findings of this study, it seems that vitamin C reduces nicotine-induced anxiety. Also, opioid receptors may be mediated of this effect of vitamin C.
 

 Introduction:
Studies have shown that pilocarpine potentiated the memory improvement induced by ethanolic extract But scopolamine attenuated memory improvement induced by ethanolic extract. In this study was investigate the Involvement of muscarinic receptors on the effect of hydroalcoholic extract of Salvia Officinalis leaves on the restraint stress- induced memory impairment has been studied.
Methods: The animals were trained in the Step-Down then were immobilized by restrainer for 60 min Immediately after training.24 and 48 hours after training, drugs were injected intra peritoneally.
48 hours after training, Retrieval testing for memory of mice was done and by recording Step-down latencies(SDL), The animals evaluated passive avoidance memory. After evaluating memory, the number of animals crossing of lines is an open field locomotor activity was measured as an indicator of measurement. After evaluating memory, the number of animals crossing of lines is an open field locomotor activity was measured as an indicator of measurement.
Results: The results showed that the restraint stress after training Immediately, reduced memory retrieval of passive avoidance memory in the test day.Two day in a row intra peritoneal injection of hydroalcoholic extract of the leaves of Salvia officinalis (60mg/kg), improve memory impairment induced by stress. The co-administration of ineffective doses of pilocarpine(1mg/Kg) with hydroalcoholic extract of the leaves of SO(40mg/kg), improve memory impairment induced by stress.On the other hand, injection of ineffective doses of scopolamine(0/5 mg/Kg) befor the test, reduced the effect of extract of the leaves SO in restoring memory impairment induced by stress. In all experiments there was no diference between the groups in terms of motor activity.
Conclution: On the basis of the results of this research it seem, restraint stress decreased the passive avoidance memory retrieval. Hydroalcoholic extract of the leaves of SO decreases the effect of restraint stress. It may concluded that the , muscarinic system mediates the effect of hydroalcoholic extract of the leaves of SO in passive avoidance memory

Introduction: Our previous studies have shown that hydroalcoholic extract of the leaves of Salvia Officinalis(SO) can reduce memory impairment induced by iron oxide nanoparticles. In this study was to investigate the involvement of opioidergic system activity in the effect of hydro alcoholic extract of the leaves of SO on memory impairment induced by iron oxide nanoparticles have been studied.
Methods: The animals were trained in the Step-down and The drugs were injected intraperitoneally (ip) immediately after training, And tested 24 hours and 7 days after training, Retrieval testing for memory of mice was done and by recording Step-down latencies (SDL), The animal was evaluated passive avoidance memory.
Results: The results showed that post-training intra peritoneal injection of iron oxide nanoparticles (5mg/kg, ip) reduced memory retrieval of passive avoidance memory in the test day. Post-training injection of hydro alcoholic extract of the leaves of SO(40mg/kg, ip) before the iron oxide nanoparticles, improved memory impairment caused by iron oxide nanoparticles. Injection of morphine(2.5mg/kg, ip), before the hydro alcoholic extract of the leaves of SO(40mg/kg, ip), reduced the effect of extract in restoring memory impairment caused by iron oxide nanoparticles. On the other hands, co-administration of ineffective doses of naloxone(0.25 mg/kg, ip) with hydro alcoholic extract of the leaves of SO(20mg/kg, ip), decreased iron oxide nanoparticles induced memory impairment.
Conclusion: On the basis of the results of this research it seem, that iron oxide nanoparticles decreases the passive avoidance memory retrieval. hydro alcoholic extract of the leaves of SO decreased the effect of iron oxide nanoparticles. It may concluded that the, opioid system mediates the effect of hydro alcoholic extract of the leaves of SO in passive avoidance memory.

 

<p>In this research, the involvement of GABA-A receptors in the effect of hydro-alcoholic extract of Salvia Officinalis (sage) leaves on iron oxide nanoparticles-induced memory impairment was studied in adult male mice.The animals were trained in the step-through inhibitory avoidance and were tested 24 hours and one week after the step-through training session for assessment of memory by recording Step-through latency.<br /> The result showed that intraperitoneal (ip) administration of iron oxide nanoparticles (5 mg/kg) immediately after training, impaired retrieval of memory. Post-training injection of GABA-A receptor antagonist, bicuculline (0.5 mg/kg), before the administration of iron oxide nanoparticles (5 mg/kg), decreased the impairment effect of iron oxide nanoparticles on memory retrieval. Post-training of co-administration of ineffective doses of bicuculline (0.125, 0.25 mg/kg) and sage (20 mg/kg)(before injection of 5 mg/kg iron oxide nanoparticles), which alone cannot improve the effect of iron oxide nanoparticles on memory, could strengthen each other's effect and increase the memory retrieval.<br /> On the Other hands, Post-training of administration of sage (40 mg/kg), before the injection of iron oxide nanoparticles (5 mg/kg), decreased the impairment effect of iron oxide nanoparticles on memory. The injection of GABA-A receptor agonist, muscimol (0.5 mg/kg), before the administration of sage (40 mg/kg), inhibited the improving effect of sage on iron oxide nanoparticles-induced memory impairment. <br /> Based on the present results, it seems that iron oxide nanoparticles are impaired passive avoidance memory and hydro-alcoholic leaves extraction of Salvia Officinalis is decreased this effect of iron oxide nanoparticles. On the other hands, activation of GABA-A Receptors related mechanisms may be involved in this effect of Salvia Officinalis.<br /> &nbsp;</p>

 

Nicotine has different effects on anxiety. High and low doses of nicotine have anxiogenic and anxiolytic effects, respectively. On the other hand, testosterone decrease anxiety and GABAergic system has an important role in anxiety behavior .The aim of this study was to determine the involvement of GABA-A receptors in the effect of testosterone on anxiogenic effect of nicotine.
In this study 180 adult male NMRI mice (in the weight: 25-30 g) were used. The animals received saline (10 ml/kg), nicotine (0.8 mg/kg), Testosterone (6.25, 12.5, 25, mg/kg), bicuculin(0.5, 1, 2 mg/kg), as intraperitoneally. Anxiety behavior of animal was evaluated by elevated plus maze and hole-board apparatus, 30 min after injection of drugs. Percentage of time spent in open arm (OAT %) and the percentage of open arm entries (OAE %)(in elevated plus maze) and the first hole-board latency and head dipping(hole-board) of animals were recorded as indices for assessment of anxiety.
The results indicated that nicotine (0.8 mg/kg) induced anxiety behavior in animals and injection of testosterone(6.25, 12.5, 25 mg/kg) decreased anxiety as dose dependently. Injection of bicuculline(0.5, 1, 2 mg/kg) had no effect on anxiety. Injection of ineffective doses of testosterone (12.5mg/kg), before nicotine, decreased anxiogenic effect of nicotine. Bicuculin (1 mg/kg) that alone had no effect on anxiety, decreased the improvement effect of the testosterone on nicotine -induced anxiogenic effect.
Based on this research, anxiogenic effect of nicotine and anxiolytic effect of testosterone are confirmed. On the other hands, testosterone is reduced nicotine-induced anxiety behavior. It seems that GABA-A receptors may also be involved in the effect of testosterone on nicotine-induced anxiety behavior.