ABSTRACT
Background and Aim: Endogenous opioids and addictive opiate drugs change many body functions. Previous studies have referred to the effects of morphine on smooth and pulmonary muscles, but the effects of opioids on skeletal muscles is not known well. Thus, the current study aimed at assessing the effect of a single dose of morphine on muscle fatigue in male rats
Materials and Methods: In this experimental study, 40 male Wistar rats weighing 220-270 g were randomly divided into four equal groups: control [the mice were kept in their cages and received food and water], morphine receiving group, fatigue group [the mice in this group were kept running on a treadmill. for120 minutes at a rate of 20 meters per minute], and morphine plus fatigue group. At the end of the experiments, blood samples were obtained from the corner of their eyes and were sent to the laboratory for measurement of muscle fatigue indexes including lactate dehydrogenase [LDH] and creatine phosphokinase [CPK]
Results: Administration of morphine to the fatigue group decreased running time compared with the control group [P=0.009]. Furthermore, administration of morphine to the fatigue group significantly increased serum levels of LDH [P=0.009] and CPK [P=0.008]
Conclusion: The present study showed that administration of a single dose of morphine in rats increases muscle fatigue biomarkers [LDH, CPK]
ABSTRACT
Introduction: Lower level of estrogen hormone is considered as an important factor for loss of learning and memory in postmenopausal women. Although estrogen replacement therapy is used for compensation, but long-term usage of estrogen is associated with a higher risk of hormone-dependent cancers. Phytoestrogens, due to fewer side effects, have been proposed to prevent menopause-related cognitive decline
Methods: 24 female Wistar rats weighing 180-220 g were used in this study. The animals were ovariectomized and randomly divided into four groups including, control and two groups which received 8 and 80 mg/kg Vitex agnus castus [VAC] ethanolic extract orally. The last groups were treated with 40 micro g/kg of estradiol valerat. Step-through passive avoidance [STPA] test was used for the evaluation of learning and memory. The hippocampal estrogen receptor alpha [ERalpha] expression was measured using Real-Time PCR
Results: The results demonstrated that VAC extract or estradiol had better performance on step-through passive avoidance test than control group [all P<0.05]. Moreover, administration of either estradiol or VAC extract increased the hippocampal mRNA level of ER alpha and prevented the decrease in uterine weight of ovariectomized rats
Discussion: Based on our data, VAC extract improves learning and memory in ovariectomized rats. The positive effect of VAC extract on learning and memory is possibly associated with an increase in ER alpha gene expression in the hippocampal formation
ABSTRACT
Background: Chronic use of opioids usually results in physical dependence. The underlying mechanisms for this dependence are still being evaluated. Transient receptor potential vanilloid type 1 [TRPV1] are important receptors of pain perception. Their role during opioid dependence has not been studied well. The aim of this study was to evaluate the effect of morphine-dependence on the expression of TRPV1 receptors in the amygdala and CA1 region of the hippocampus
Methods: This study used four groups of rats. Two groups of rats [morphine and morphine+naloxone] received morphine based on the following protocol: 10 mg/kg [twice daily, 3 days] followed by 20, 30, 40 and 50 mg/kg [twice daily], respectively, for 4 consecutive days. Another group received vehicle [1 ml/ kg] instead of morphine given using the same schedule. The morphine+naloxone group of rats additionally received naloxone [5 mg/kg] at the end of the protocol. The control group rats received no injections or intervention. The amygdala and CA1 regions of the morphine, saline-treated and intact animals were isolated and prepared for real-time PCR analysis
Results: Administration of naloxone induced withdrawal signs in morphine-treated animals. The results showed a significant decrease in TRPV1 gene expression in the amygdala [P<0.05] but not the CA1 region of morphine dependent rats
Conclusion: TRPV1 receptors may be involved in morphineinduced dependence
ABSTRACT
Background: Transient global cerebral ischemia causes extensive neuronal damage in the brain and leads to a deficit in learning and memory. We designed the present study to investigate the effect of exercise preconditioning on learning and spatial memory following transient cerebral ischemia in rat
Materials and methods: In this experimental study, 50 male Wistar rats weighing 250-300g were randomly allocated to different groups. Exercise was done by treadmill and, for inducing cerebral ischemia, both common carotid arteries were occluded for 10 minutes. Memory was evaluated using a step-through passive avoidance task. Sensory motor deficits were assessed by adhesive removal test. For evaluating slip ratio, we used ledged beam walking test
Results: One week after transient cerebral ischemia, response latency decreased in passive avoidance test. Also touch time, remove time, and slip ratio were increased in these animals. Exercise preconditioning improved the measured indices in ischemic rats
Conclusion: Exercise preconditioning improved deficits in learning and memory, as well as sensory-motor function, following transient cerebral ischemia
ABSTRACT
Morphine addiction and morphine withdrawal syndrome are the two main problems of today's human society. The present study has investigated the effects of nicotine on the strength of physical and psychological dependency in single and repeated doses morphine administrated rats. Male Wistar rats were subjected to morphine consumption with single or frequent dose protocols. In the single dose protocol, rats received only one dose of morphine and 24hrs later they also received one dose of nicotine 30 min prior to injection of naloxone. In the repeated dose protocol, rats received incremental doses of morphine for 7 days and 24hr after the last dose [the 8th day] were given naloxone. However, the nicotine regimen of this group was injected 15 min before the morphine injection, for 4 days, from the 4th to the 7th day. Five minutes after naloxone injection, each rat's behavior was captured for 30 min, and then physical and psychological signs of withdrawal syndrome were recorded. Data were analyzed by ANOVA followed by Tukey tests and p<0.05 was considered as significant difference. Results showed that the injection of frequent and single doses of morphine lead to morphine dependency. In single dose protocol, nicotine consumption attenuated the signs of withdrawal syndrome, especially weight of excrement and total withdrawal score. In frequent dose protocol, in addition to these effects, nicotine induced weight loss and place aversion. The inhibitory effects of nicotine on signs of withdrawal syndrome may involve a dopaminergic portion of the central nervous system and is mediated by central nicotinic receptors. There is also a cross-dependence between nicotine and morphine