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Crack is a solid salt processed with sodium bicarbonate from cocaine. Methamphetamine is a derivative of methylamphetamine, which is highly addictive. The current study aims to investigate the effect of intraperitoneal injection of crack cocaine and methamphetamin over the parameters of blood creatinine, urea, sodium, and potassium as indicators of kidney failure in male rats.

This experimental study was carried out over seven groups of 6 male rats, including a control group, three crack-cocaine experimental groups, and three methamphetamine experimental groups, each of them receiving concentrations of 5, 10, and 15 mg/kg of crack-cocaine or methamphetamine respectively for 7 days (once a day). After the drug injection, blood was taken from the hearts of the rats and the parameters of urea, sodium, potassium, and creatinine were measured and analyzed from the blood samples taken. Statistical analysis of the data was done with the one-way analysis of variance and Tukey's post hoc test via SPSS.

The injection of low and medium concentrations of two drugs, crack cocaine and methamphetamine, had no significant effect on the mentioned parameters (P > 0.05), and only the medium concentration of methamphetamine caused the amount of blood potassium to increase compared to the control group (P < 0.05). Injection of 15 mg/kg concentration of both drugs significantly increased the amount of blood creatinine in the respective groups (P < 0.05).

The increase in plasma creatinine due to the administration of methamphetamine and crack-cocaine may be caused by acute renal failure, rhabdomyolysis, or the induction of acute interstitial nephritis.

 Acute and chronic effects of nitric oxide on oxidative stress and neuronal demyelination have been reported in human and animal models. 

 Oxidative stress is involved in the pathogenesis of demyelinated animals; thus, this study investigated the effects of nitric oxide system and ethidium bromide on oxidative stress in the hippocampal formation.  

 This experimental study was performed on eight groups of male rats, as follows: control, control, ethidium bromide, L-Arginine, L-NAME, ethidium bromide + L-Arginine, ethidium bromide + L-NAME, and ethidium bromide + L-Arginine + L - NAME. Three days after the injection of drugs into the hippocampal CA1 area, hippocampal biopsy was performed, and oxidative stress parameters were measured in this area. One-way analysis of variance (ANOVA) and posthoc tests were used for data analysis.

 Injection of 3 μL ethidium bromide into the CA1 region increased oxidative stress parameters (P<0.01). Injection of 15.3 μg/rat L-Arginine in this region stopped the response of ethidium bromide (P<0.05, P<0.01); while, the injection of 15.1 μg/rat L-NAME failed to return the effects of the ethidium bromide. Moreover, the combination of 15.3 μg/rat L-Arginine and 15.1 μg/rat L-NAME only returned lipid peroxidation caused by the injection of 3 μL of ethidium bromide to normal (P<0.05); this process failed to improve antioxidant enzymes.

 The obtained results suggested the excitatory effect of the nitric oxide system on alleviating oxidative stress induced by ethidium bromide in the CA1 region of male rats.

The aim of this study was to investigate the effect of short-term microinjection of Ferula szowitsiana extract on the process of spatial memory and lipid peroxidation in the hippocampus in an experimental model of Multiple Sclerosis (MS). In this experimental study, 35 male Wistar rats were randomly divided into five groups. Each group has 7 rats. These groups were included control, sham, model of MS and MS groups with plant extract treatments. In the experimental model of MS groups, induction of MS was carried out by single injection of ethidium bromide (EB) into the hippocampus. One week after MS induction by EB (0.01 %), the MS groups were treated by Ferula szowitsiana extract (5 and 10 μg/rat) for 3 consecutive days. Finally following the treatment period, for measuring spatial memory, Morris Water Maze test was carried out and the hippocampus of both sides were dissected and used for measurement of Malondialdehyde (MDA). The results showed that in the experimental model of MS group travelled distance (1022.44±53.29) and escape latency (41.30±3.29) increased compared to travelled distance (885.94±29.56) and escape latency (36.26±0.65) in the control group (p<0.001). Short-term treatment by Ferula szowitsiana extract in this models decreased the travelled distance (838.39±24.16) and escape latency (39.87±1.24) (P<0.001). MDA increased in the experimental model of MS group (3.8±0.51) compared to the control group (0.68±0.13) (p<0.001) and in the Ferula treated group (0.34±0.04) decreased compared to the MS animals (P<0.001). Treatment with Ferula szowitsiana extract is able to prevent memory and learning reduction, through inhibition of lipid peroxidation in an experimental model of MS.

Beside its autonomic functions, the nucleus paragigantocellularis lateralis (LPGi) is involved in the descending pain modulation. 17β-Estradiol is a neuroactive steroid found in several brain areas such as LPGi. Intra-LPGi microinjection of 17β-estradiol can elicit the analgesic responses. 17β-Estradiol modulates nociception by binding to estrogenic receptors as well as allosteric interaction with other membrane-bound receptors like GABAA receptors. This study aimed to examine the role of GABAA receptors in the pain modulating effect of intra-LPGi injection of 17β-estradiol.
To study the antinociceptive effects of 17β-estradiol, cannulation into the LPGi nucleus of male Wistar rats was performed. About 500 nL of drug was administered 15 minutes prior to formalin injection (50 μL of 4%). Then, formalin-induced flexing and licking behaviors were recorded for 60 minutes. For evaluating the role of GABAA receptors in the estradiol-induced pain modulation, 17β-estradiol was administered into the LPGi nucleus 15 minutes after the injection of 25 ng/μL bicuculline (the GABAA receptor antagonist). Then, the formalin-induced responses were recorded.
The results of the current study showed that intra-LPGi injection of 17β-estradiol decreased the flexing duration in both phases of formalin test (P According to the results of this study, the analgesic effect of intra-LPGi 17β-estradiol on the formalin-induced inflammatory pain might be mediated via GABAA receptors.

17β-Estradiol modulates nociception by binding to the estrogenic receptors and also by allosteric interaction with other membrane-bound receptors like glutamate and GABAA receptors. In addition to its autonomic functions, paragigantocellularis lateralis (LPGi) is involved in the pain modulation, too. The aim of the current study was to investigate the involvement of the membrane-bound GABAA receptors in the pain modulatory effect of intra- LPGi injection of 17β-estradiol of male rats. This study was performed using male Wistar rats in the range of 200-270 g. In order to investigate the antinociceptive effect of intra-LPGi microinjection of 17β-estradiol, cannulation into the LPGi nucleus was performed. 500 nl of drugs were administered 15 minutes prior to formalin injection (50 μl of 4%). Then, formalin-induced paw jerking behaviour was recorded for 60 min. For assessing the role of the GABAA receptors in the estradiol induced pain modulation, 17β-estradiol was administered into the LPGi nucleus 15 min after the injection of 25 ng/μl bicuculline; and paw jerking frequency was recorded for 1 h. The results of the current study showed that intra-LPGi injection of 0.8 μmol of 17β-estradiol attenuated the chronic phase (P<0.001) of paw jerking behaviour. Bicuculine -the GABAA receptor antagonist- significantly reduced the antinociceptive effect of intra-LPGi 17β-estradiol in the chronic phase (P<0.001). It may be concluded that the analgesic effect of intra-LPGi injection of 17β-estradiol on the formalin-induced inflammatory pain might be mediated via GABAA receptors.

17β-estradiol modulates nociception by binding to estrogenic receptors and also by allosteric interaction with other membrane-bound receptors like glutamate and GABAA receptors. Beside its autonomic functions, paragigantocellularis lateralis (LPGi) nucleus is also involved in pain modulation. The aim of the current study was to investigate the role of the intracellular estrogenic receptors in the pain modulation by the LPGi nucleus of male rats. In this study, male Wistar rats in the range of 200-270 gr were used. In order to study the effect of intra- LPGi microinjection of 17β-estradiol on both acute and persistent pain modulation, cannulation of LPGi nucleus was performed. At first, drugs were injected and 15 minutes later 50 μl of 4% formalin was injected into the rat's hind paw. Then formalin-induced flexing and licking behaviours were recorded for 60 min. The results of current study showed that intra-LPGi injection of 17β-estradiol attenuated the flexing and the licking behaviours both in the first phase (P<0.01) and in the second phase (P<0.001) of formalin test. The estrogen receptor antagonist (ICI182,780) prevented 17β-estradiol-induced analgesic effect but could not reverse this effect to the control condition, and it had significant difference with the control group, yet. It may be concluded some part of the analgesic effect of 17β-estradiol in the LPGi nucleus on the formalin-induced inflammatory pain is probably mediated by estrogenic receptors.

Ecstasy is an amphetamine derivative, which its use has been consistently increasing over the past years. Ecstasy interacts with the glutamatergic system and it is known that glutamate receptors have a key role in learning and memory. The aim of this study was to investigate the interaction of ecstasy and glutamatergic system on learning and memory. Fifty-six male Wistar rats weighting (250±50 g) were randomly divided into 8 groups, which received injections for 7 consecutive days. Spatial memory was assessed using Morris Water Maze, performed for 5 consecutive days after the treatment period. The swim speed showed no significant difference among the groups. The mean latency time in finding the hidden platform was increased during test trial in the ecstasy, MK-801 (a glutamate antagonist) and ecstasy + MK-801 groups compared to the control (P < 0.05), while it was decreased during test trial in ecstasy, NMDA and ecstasy + NMDA groups compared to the control (P< 0.05). The mean latency distance in finding the hidden platform was increased during test trial in ecstasy, MK-801 and ecstasy + MK-801 groups compared to the control (P < 0.05), and decreased during test trial in ecstasy, NMDA and ecstasy + NMDA groups compared to the control (P<0.05). Results showed that ecstasy with NMDA treatment attenuated the reduced spatial memory by ecstasy. Ecstasy with MK-801 potentiated the reduced spatial memory by ecstasy.

17β-Estradiol is a neuroactive steroid and its pain modulatory role has been well studied previously. 17β-Estradiol modulates nociception by binding to its receptors and also by allosteric interaction with other membrane - bound receptors such as glutamate and GABAA receptors. Paragigantocellularis lateralis (LPGi) is also involved in pain modulation and perception, in addition to its well-known autonomic functions such as regulation of circulation. In order to study the effect of intra-LPGi injection of 17β-estradiol on both acute and persistent pain, 50 μl of 4% formalin was injected into the male rats’ hind paw, then fo rmalin-induced paw jerking behaviour was recorded for 60 min. The results of this study indicated that intra-LPGi injection of 17β-estradiol attenuated the second phase, but not the acute phase of formalin induced pain (P< 0.001). The estrogen receptor antagonist (ICI182,780) counteracted 17β-estradiol’s effect, but could not reverse the antinociceptive effect of 17β -estradiol to its basic level. It may be concluded that a part of the analgesic effect of 17β-estradiol in formalin induced inflammatory pain is mediated by intracellular estrogen receptors; the other part of this effect is possibly mediated through allosteric interactions with other membrane-bound receptors such as glutamate and GABAA receptors.

Cognitive dysfunction is recognized as a significant feature of multiple sclerosis (MS). Oxidative stress plays an important role in the pathogenesis of MS. Toxic demyelination by ethidium bromide (EB) is one of the common methods for induction of MS, which leads to neuronal death by production of free radicals and enhancement of oxidative stress burden. According to previous pharmacological studies, saffron extract acts as a free radical scavenger. Accordingly, in the present study the effect of short-term microinjection of saffron extract on the process of spatial memory and lipid peroxidation in the hippocampus was assessed in an experimental model of MS.

One week after MS induction by EB (0.01 %), animals of the experimental group were treated by saffron extract (5 and 10 μg/rat) for 3 consecutive days. Following the treatment period, Morris Water Maze test was carried out and hippocampi of both sides were dissected and used for measurement of a lipid peroxidation marker (MDA) in the end.

Based on the results of the present study, short-term treatment by saffron extract significantly ameliorated spatial memory in experimental models of MS (P<0.05). MDA in the saffron treated group showed a significant reduction compared to the control MS animals (P<0.01).

It seems that treatment with saffron extract is able to prevent memory and learning reduction, through inhibition of lipid peroxidation in an experimental model of MS. However, evaluation of beneficial effects of saffron on the spatial memory and its role in preventing or treating cognitive deficits in MS patients, requires much more extensive molecular studies.