Basic and Clinical Neuroscience
Volume:4 Issue: 4, Autumn 2013

Transplantation of bone marrow stromal cells (BMSCs) or Schwann cells (SCs) can increase axonal regeneration in peripheral nerve injuries. Based on our previous investigations, the goal of the present work was to examine the individual and synergistic effects of the two different cell types in sciatic nerve injury. We pursued to evaluate the effects of BMSCs and SCs co-transplantation on the functional recovery after sciatic nerve injury in rat. In this experimental research, adult male Wistar rats (n=32, 250-300g) were used, BMSCs and SCs were cultured, and the SCs were confirmed with anti S100 antibody. Rats were randomly divided into 4 groups (n=8 in each group): 1- control group: silicon tube filled with fibrin gel without cells; 2- BMSCs group: silicon tube filled with fibrin gel seeded with BMSCs; 3- SCs group: silicon tube filled with fibrin gel seeded with SCs and 4- co-transplantation group: silicone tube filled with fibrin gel seeded with BMSCs and SCs. The left sciatic nerve was exposed, a 10 mm segment removed, and a silicone tube interposed into this nerve gap. BMSCs and SCs were transplanted separately or in combination into the gap. BMSCs were labeled with anti-BrdU and SCs were labeled with DiI. After 12 weeks electromyographic and functional assessments were performed and analyzed by one-way analysis of variance (ANOVA). Electromyographic and functional assessments showed a significant difference between the experimental groups and controls. Electromyography measures were significantly more favourable in SCs transplantation group as compared to BMSCs transplantation and co-transplantation groups (p<0.05). Functional assessments showed no statistically significant difference among the BMSCs, SCs and co-transplantation groups (p<0.05). Transplantation of BMSCs and SCs separately or in combination have the potential to generate functional recovery after sciatic nerve injury in rat. The electromyography evaluation showed a greater improvement after SCs transplantation than BMSCs or the co-transplantation of BMSCs and SCs.

Considering the prevalence of epilepsy and the failure of available treatments for many epileptic patients, finding more effective drugs in the treatment of epilepsy seems necessary. Oxidative stress has a special role in the pathogenesis of epileptic syndrome. Therefore, in the present study, we have examined the anti-epileptic and anti-oxidant properties of the Ferula Assa Foetida gum extract, using the pentylentetrazole (PTZ) kindling method. group which received valproate (100 mg/kg) as anti-convulsant drug, 4-5 & 6- the groups of kindled mice that pretreated with 25, 50 and 100 mg/kg doses of Ferula Assa Foetida gum extract. Kindling has been induced in all groups, except for the control group via 11 PTZ injections (35 mg /kg; ip) every other day for 22 days. In the 24th day, the PTZ challenge dose was injected (75 mg / kg) to all groups except the control group. The intensity of seizures were observed and noted until 30 minutes after PTZ injection. At list, the mice were decapitated and the brains of all the mice were removed.. and their biochemical factors levels including malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were determined. Results of this study show that Ferula Assa Foetida gum extract is able to reduce seizure duration and its intensity. In addition, this extract has reduced MDA and NO levels and increased the level of SOD in the brain tissue compared to the PTZ- kindled mice. It can be concluded that Ferula Assa Foetida gum extract, in specific doses, is able to show an anti-epileptic effect because of its antioxidant properties, probably acting through an enzyme activity mechanism. In this experimental study, sixty male Albino mice weighing 25-30 g were selected and were randomly divided into 6 groups. 1- the control group, 2- PTZ-kindled mice, 3- positive control

Addiction imposes a large medical, social and economic burden on societies. Currently, there is no effective treatment for addiction. Our struggle to decipher the different mechanisms involved in addiction requires a proper understanding of the brain regions which promote this devastating behavior. Previous studies have shown a pivotal role for insula in cigarette smoking. In this study we investigated the change in opium consumption after CVA. This study took place in three referral academic hospitals affiliated to Tehran University of Medical Sciences. Patients who suffered a CVA and were addicted to opium were recruited during their hospitalization or visit to the neurology clinic in this study. Age, sex and the route and mean amount of opium use of each patient before CVA and 1, 3 and 6 months post-CVA was asked using a questionnaire. The patients were divided into three groups based on the location of brain ischemia (insula, basal ganglia and non-insula non-basal ganglia group). Seventy five percent of the patients with ischemia of the insula changed the route or amount of opium use after CVA and 37.5% of them stopped opium use after CVA. These values were significantly higher than patients with non-insula non-basal ganglia ischemia (p values 0.005 and 0.03 for change in route or amount and stopping opium use, respectively). This was not true in patients with ischemia of the basal ganglia. Younger patients were more likely to change the route or amount of opium use and stop opium use after CVA (p values 0.002 and 0.026, respectively). The results of the present study indicate a possible role for the insula in opium addiction, especially in younger individuals.

One of the hallmark symptoms of posttraumatic stress disorder (PTSD) is the impaired extinction of traumatic memory. Single prolonged stress (SPS) has been suggested as an animal model of PTSD, since SPS rats exhibited the impaired fear extinction. Oxytocin (OXT) has been recently suggested as a potential pharmacotherapy for treatment of PTSD. In this study, using SPS rats we investigated the effects of multiple systemic administration of OXT on contextual fear extinction. SPS was conducted in three stages: restraint for 2 h, forced swim for 20 min, and diethyl ether anesthesia, and then left undisturbed in their home cage for 7 days. In the SPS group, 7 days after SPS treatment, contextual fear conditioning was performed (on day 0), and then extinction training was performed on each of four consecutive days following fear conditioning. In the sham group, the procedures were similar except that SPS treatment was not performed. During extinction trial (10 min) freezing behavior was recorded. OXT (1, 10, 100 and 1000μg/kg) was administrated (I.P) immediately after each extinction trial. SPS rats exhibited significant impairment of contextual fear extinction as compared with sham rats. While there was no significant difference in the freezing levels between SPS and Sham rats 24 h after the fear conditioning, the freezing levels in SPS rats were significantly higher than those in sham rats after the second extinction training. Systemic OXT delayed fear extinction in sham rats as compared with sham-saline treated animals. No effect of OXT was found in SPS rats. These findings indicate that increasing OXT transmission during fear memory reactivation delays fear extinction, and thus, the recommendation of OXT for PTSD treatment should be considered with caution.

Colchicine, a potent neurotoxin derived from plants, has been recently introduced as a degenerative toxin of small pyramidal cells in the cortical area 1 of the hippocampus (CA1). In this study, the effect of the alkaloid in CA1 on the behaviors in the conditioning task was measured. Injections of colchicine (1,5 μg/rat, intra-CA1) was performed in the male Wistar rats, while the animals were settled and cannulated in a stereotaxic apparatus. In the control group solely injection of saline (1 μl/rat, intra-CA1) was used. One week later, all the animals passed the saline conditioning task using a three-day schedule of an unbiased paradigm. They were administered saline (1 ml/kg, s.c.) twice a day throughout the conditioning phase. To evaluate the possible effects of cell injury by the toxin on the pyramidal cells, both the motivational signals while in the conditioning box and the non-motivational locomotive signs of the treated and control rats were measured. Based on the present study the alkaloid caused no change in the score of place conditioning, but affected both the sniffing and grooming behaviors in the group that received colchicine. However, the alkaloid did not show the significant effect on the rearing or compartment entering in the rats. According to the findings, the intra-CA1 injection of colchicine may impair the neuronal transmission of non-motivational information by the pyramidal cells in the dorsal hippocampus.

Exposure to 3-4, methylenedioxymethamphetamine (MDMA) leads to cell death. Herein, we studied the protective effects of ginger on MDMA- induced apoptosis. 15 Sprague dawley male rats were administrated with 0, 10 mg/kg MDMA, or MDMA along with 100mg/kg ginger, IP for 7 days. Brains were removed to study the caspase 3, 8, and 9 expressions in the hippocampus by RT-PCR. Data was analyzed by SPSS 16 software using the one-way ANOVA test. MDMA treatment resulted in a significant increase in caspase 3, 8, and 9 as compared to the sham group (p<0.001). Ginger administration however, appeared to significantly decrease the same (p<0.001). Our findings suggest that ginger consumption may lead to the improvement of MDMA-induced neurotoxicity.

Gap junctions are intercellular membrane channels that provide direct cytoplasmic continuity between adjacent cells. This communication can be affected by changes in expression of gap junctional subunits called Connexins (Cx). Changes in the expression and function of connexins are associated with number of brain neurodegenerative diseases. Neuroinflammation is a hallmark of various central nervous system (CNS) diseases, like multiple sclerosis, Alzheimer''s disease and epilepsy. Neuroinflammation causes change in Connexins expression. Hippocampus, one of the main brain regions with a wide network of Gap junctions between different neural cell types, has particular vulnerability to damage and consequent inflammation. Cx32 – among Connexins– is expressed in hippocampal Olygodandrocytes and some neural subpopulations. Although multiple lines of evidence indicate that there is an association between neuroinflammation and the expression of connexin, the direct effect of neuroinflammation on the expression of connexins has not been well studied. In the present study, the effect of neuroinflammation induced by the Lipopolysaccharide (LPS) on Cx32 gene and protein expressions in rat hippocampus is evaluated. LPS (2.5μg/rat) was infused into the rat cerebral ventricles for 14 days. Cx32 mRNA and protein levels were measured by Real Time PCR and Western Blot after 1st, 7th and 14th injection of LPS in the hippocampus. Significant increase in Cx32 mRNA expression was observed after 7th injection of LPS (P<0.001). However, no significant change was observed in Cx32 protein level. LPS seems to modify Cx32 GJ communication in the hippocampus at transcription level but not at translation or post-translation level. In order to have a full view concerning modification of Cx32 GJ communication, effect of LPS on Cx32 channel gating should also be determined.

The concentration of noradrenalin and corticosterone as the two nociception modulators change after fasting or stress situation. The aim of present study was to investigate the effect of food deprivation on formalin-induced nociceptive behaviours and plasma levels of noradrenalin and corticosterone in rats. Food was withdrawn 12, 24 and 48 h prior to performing the formalin test, but water continued to be available ad libitum. The formalin solution (50 μL, 2%) was injected into plantar surface of hind paw. The nociception responses of the animals during the first phase (1-7 minutes), the inter-phase (8-14), the phase 2A (15-60) and the phase 2B (61-90) was separately evaluated. The plasma concentrations of noradrenalin and corticosterone were measured using specific ELISA and IRA kits, according to manufacturer''s instructions. In contrast to the increasing of 48 h food deprived animals during phase 2, the nociceptive behaviours of 12 and 24 h groups decreased through the interphase, phase 2A and phase 2B. The injection of formalin in the normal male rats significantly decreased the plasma level of noradrenalin and corticosterone. Food deprivation for 12 and 24 h increased noradrenalin level significantly in comparison with control group which has caused by fasting induced antinociceptive behaviours. There was no significant change in food deprivation for 48 h group. Food deprivation for 12, 24 and 48 h had no effect on corticosterone level in male rats. The present study emphasizes that the acute food deprivation diminished the nociceptive behaviours in the formalin test and show a correlation with increase in plasma noradrenalin level.