Basic and Clinical Neuroscience
Volume:1 Issue: 2, Winter 2010

In the present study, interactions between lead exposure with nitric oxide precursor (L-arginine) or nitric oxide synthase (NOS) inhibitor (L-NAME) on naloxone-induced jumping and diarrhea in morphine-dependent mice were examined. Chronic lead acetate (0.05%) exposure altered naloxone-induced jumping and diarrhea in mice. Jumping was decreased after 7 days and was unchanged 14 and 28 days after lead exposure. Diarrhea was only increased 28 days after lead exposure, which shows a difference between two signs of withdrawal syndrome. Since jumping is the most important sign, the animals were exposed to lead for 7 days in the rest of experiments. In a set of experiments, the nitric oxide agents (L-arginine) or L-NG-nitro arginine methyl ester (L-NAME) were used before naloxone injection to test their effects on the expression of jumping. The low dose of L-arginine, a precursor of nitric oxide (20 mg/kg) decreased jumping, but increased diarrhea. Higher dose of L-arginine (80 mg/kg) increased jumping, while decreased diarrhea. L-NAME decreased both jumping and diarrhea. On the other hand, L-arginine in combination with lead reversed lead-induced attenuation of naloxone-induced jumping, while decreased diarrhea. L-NANE in combination with lead decreased diarrhea, while did not alter jumping. In the second set of experiments, nitric oxide drugs were injected during development of morphine dependency. Data showed that jumping was increased or decreased by low or higher dose of L-arginine respectively. Diarrhea was also increased by the drug. L-NAME decreased both jumping and diarrhea in the development of morphine dependency. Both L-arginine and L-NAME in combination with lead decreased lead-induced jumping and diarrhea. It is concluded that nitric oxide may modulate morphine withdrawal signs and lead-induced attenuation of jumping.

Patients with schizophrenia characteristically exhibit cognitive deficits. The level of cognitive impairment is found to predict the functional outcome of the illness more strongly than the severity of positive or negative symptoms. The purpose of this study was to assess the efficacy of ondansetron, a 5-HT3 receptor antagonist as an adjuvant agent in the treatment of chronic schizophrenia in particular for cognitive impairments. This investigation was a 12-week, double blind study of parallel groups of patients with stable chronic schizophrenia. Thirty patients were recruited from inpatient and outpatient departments. All participants met Diagnostic and Statistical Manual of Mental Disorders Fourth Edition, Text Revision (DSM-IV-TR) criteria for schizophrenia. To be eligible, patients were required to have been treated with a stable dose of risperidone as their primary antipsychotic treatment for a minimum period of 8 weeks. The subjects were randomized to receive ondansetron (8 mg/day) or the placebo in addition to risperidone. Cognition was measured by a cognitive battery. Patients were assessed at baseline and after 8, and 12 weeks after the medication started. Administration of ondansetron significantly improved visual memory based on improvement on visual reproduction, visual paired associate and figural memory sub tests of Wechsler Memory Scale Revised. The present study indicates ondansetron as potential adjunctive treatment strategy for chronic schizophrenia particularly for cognitive impairments.Keywords:

Introdution: Stroke is one of the most common diseases caused by occlusion or rupture of blood vessels in brain. It brings heavily loads for families and societies. Although some new strategies including treatment of tissue plasminogen activator have been applied in the clinic, these methods do not have perfect effect. Accordingly, more effective therapeutic strategies need to be developed. This study was conducted to investigate the action of bone marrow stromal cells (BMSC) on the neural stem cells in the subventricular zone of the rat after focal cerebral ischemia. The rats were induced to permanent focal cerebral ischemia models with middle cerebral artery occlusion (MCA0). Test groups consisted of three groups: MCAO alone, intravenous infusion of 1 ml PBS at 24 hours after MCAO, and intravenous infusion of 2×106 BMSCs 24 hours after MCAO. Then, the groups were divided to investigate at 7 and 14 days after MACO. Neurological functions were detected to use Zausinger evaluation; meanwhile, 5-bromodeoxyuridine was injected to label the proliferating cells in the subventricular zone, and double-immunofluoroscent technologies were used to identify the cell type. Neurological functional scores of BMSCs-treated group were higher than other two groups (p<0.05) at 7 and 14 days after MACO. BrdU-positive cells in SVZ of ipsilateral ischemia of BMSCs-treated group were more than two controls (p<0.05) at 14 days after MCAO; double-immunofluorescence label demonstrated that BrdU-positive cells co-located with markers of neuron and astrocyte. BMSCs can promote the neurological function of the rats with permanent focal cerebral ischemia, which may associate with the neurogenesis in the subventricular zone.

Social inequality may have a significant negative effect on health. There are some evidences that social inequality and stressful conditions could lead to development and progression of various disorders. On the other hand, the results of some research studies have shown that reducing the consumed calorie could prolong the lifetime. In addition, limiting the consumed calorie could produce beneficial changes in the level of some hormones including blood insulin and may reduce body temperature. Meanwhile, food restriction could reduce genetic damage and may have protective effect against external toxins. Therefore, the aim of the present study was to evaluate the effect of food restriction on learning and memory of male rats using passive avoidance and Y-maze tests. For this purpose, male Wistar rats (n = 48) were divided into control, 3 experimental, and two negative and positive control groups. Control group received normal rat regimen for 6 weeks. The group with full restriction and non-isolated received 1/3 of the food regimen. The group with full restriction and isolation received 1/3 of the food regimen. The experimental group with two-weeks food restriction and non-isolated received 1/3 of the food regimen only for two weeks. Streptozotocin-diabetic rats with blood glucose higher than 250 mg/dl was considered as negative and positive control received vitamin E (10 mg/kg/day; i.p.) as an antioxidant. For evaluation of learning and memory, initial and step-through latencies and alternation behavior were analyzed using passive avoidance and Y-maze tests. Regarding initial latency, there was a reduction in diabetic, vitamin-E treated, and group with 2-weeks food restriction and there was an increase in groups with full restriction and isolated and with full restriction as compared to control. Meanwhile, there were no significant differences among the groups, indicating that there were no changes in behavior acquisition. With respect to step-through latency which indicates the ability for consolidation and recall of information, vitamin-E treated group and group with full restriction showed a slight non-significant increase as compared to control group. Diabetic group showed a significant reduction (p<0.01) in comparison with control group. Meanwhile, in groups with full restriction and isolated and with 2-weeks restriction showed a significant reduction in relation to control group (p<0.05 and p<0.01). In addition, these groups showed a significant higher index as compared to diabetic group (p<0.05). The results of Y-maze which indicated spatial memory capability of the animal showed that alternation was significantly lower in diabetic group as compared to control (p<0.01) and there was no significant differences for other groups as compared to control. On the other hand, vitamin E caused a slight increase in this regard. The results of this study showed that food restriction irrespective of intervention kind did not produce a significant change regarding behavior acquisition and full food restriction (non-isolated) also did not cause a significant change regarding animal ability for consolidation and recall of information in relation to control group. Meanwhile, 2-weeks restriction and full restriction with isolation caused a significant reduction in this respect. In addition, food restriction did not have an effect on spatial memory.

In this study, 22 patients (15-75 years old) were selected and transferred to CT scan for tumor ablation. For ablations, after prep and drep under the local anesthesia and mild sedation in proper position, small incision made and special needle inserted and guided by proper direction to the core of the tumor. Then, laser probe inserted through the needle and laser energy delivered. Although we have not a good prognosis in metastatic tumors but post-operative follow up and brain CT scan established the effect of laser on resection and evaporation and diminution of mass effect in tumor lesions.

A large body of experimental evidence supports a role for oxidative stress as a mediator of nerve cell death in Parkinson's disease (PD). Flavonoids like quercetin have been reported to prevent neuronal degeneration caused by increased oxidative burden, therefore, this study examined whether quercetin administration at a high dose would attenuate behavioral abnormalities in experimental model of PD in rat. For this purpose, unilateral intrastriatal 6-hydroxydopamine (6-OHDA)-lesioned rats were pretreated with quercetin (20 mg/kg; i.p.) 1 hour before surgery and treated once a day for one month. After one month, apomorphine-induced rotational behavior was measured postlesion. Apomorphine-induced rotations were counted after 4 weeks. Quercetin administration could attenuate the rotational behavior in treated lesioned rats as compared to untreated ones. Flavonoid quercetin administration for one month could attenuate behavioral abnormalities in 6-OHDA model of PD.

This study was conducted to determine the possible beneficial results of L-arginine on prefrontal cortex of rats which impressed by immobilization stress to define the synchronous impression of stress and nitric oxide (NO) on evolution of prefrontal cortex of rats after birth. Forty-eight one month, male Wistar rats were divided into two groups: stressed and non-stressed. L-Arginine (200 mg/kg) as a NO synthase (NOS) inducer and L-NAME (2O mg/kg) were injected intraperitonealy (IP) and 7- nitroindazde (25 mg/kg) as non-specific was injected subcutaneously (S.C.) for 4 weeks. The kind of stress was immobilization for 4 weeks, every other day. The brain was removed after this period and each brain divided into two parts in a coronal section manner. Anterior part used for histological studies with H&E staining and posterior part used for measurement of NO production using spectrophotometer at 540 nm wavelengh. Statistical analysis of microscopic and light microscopic finding showed that thickness of prefrontal cortex and NO production were significantly decreased in stressed rats and especially in groups which received 7- nitroindazole and L-NAME and L-arginine could reverse these results. According to this research, we could say that L-arginine decreases the cortical damages in stressed rats and 7-nitroindazole and L-NAME increase this damage in non-stressed group. Although in non stressed groups, L-arginine, L-NAME and 7- nitroindazole were all non-protective and damaging.

This study was designed to investigate the effects of granulocyte colony-stimulating factor (G-CSF) administration in rats for 6 weeks after traumatic brain injury (TBI). Adult male Wistar rats (n = 30) were injured with controlled cortical impact device and divided into four groups. The treatment groups (n = 10 each) were injected subcutaneously with recombinant human G-CSF. Vehicle group (n=10) received phosphate buffered saline (PBS) and only Brdu intraperitoneally. Bromodeoxyuridine (BrdU) was used for mitotic labeling. Experimental rats were injected intraperitoneally with BrdU. Rats were killed at 6th week after traumatic brain injury. Neurological functional evaluation of animals was performed before and after injury using neurological severity scores (NSS). Animals were sacrificed 42 days after TBI and brain sections were stained using Brdu immunohistochemistry. Statistically significant improvement in functional outcome was observed in treatment groups when compared with control (p<0.01). This benefit was visible 7 days after TBI and persisted until 42 days (end of trial). Histological analysis showed that Brdu cell positive was more in the lesion boundary zone at treatment animal group than all injected animals. We believe that G-CSF therapeutic protocol reported here represents an attractive strategy for the development of a clinically significant noninvasive traumatic brain injury therapy.