Chronic exposure to Lead (Pb) affects neural functions in central nervous system (CNS) particularly the learning and memory. On the other hand, alteration of calcium level in the CNS results in activation of NOS where it is expected to increase nitric oxide level in hippocampus. In this study the role of Lead exposure in NMDA induced NO production in PYRAMIDAL hippocampal CELLS (CA1HP) was investigated. The NO level was determined by measurement of concentration of nitrite and nitrate as NO products using the metHb production at 401 nm. The ACBD (NMDA agonist)-induced NO level was almost reduced to the control level (2.5 nM) in the presence of 10 and 100 nM of Lead acetate. Lead acetate at concentrations which normally results in chronic toxicity did not increase the nitric oxide (NO) production by CA1HP. One reason for this finding could be the interaction of Lead with NMDA receptors due to similarity of Pb2+ to Zn2+ ion. Another reason may be related to direct interaction of Lead with NMDA receptors that inhibit the stimulated NO production.

Background: Ecstasy or 3-4, methylenedioxymethamphetamine (MDMA), as an amphetamine derivate, could lead to learning and memory impairment.Objectives: As the hippocampus is responsible for learning and memory, herein we evaluated acute and chronic effects of MDMA on the structure of the hippocampus.Materials and Methods: Male Wistar rats (200-250 g) received single or multiple injections of MDMA (10 mg/kg, IP). At the end of the study, rats were killed and their brains were removed. Hippocampus sections were prepared to study the structure of hippocampus CA1. Data was analyzed using SPSS 16 software and one-way analysis of variance test.Results: Our findings showed that cell density decreased in MDMA-treated groups in comparison to the intact group. Administration of multiple doses of MDMA significantly decreased the cell number when compared with intact (P<0.001) and acute (P<0.01) groups.Conclusions: These data suggest that MDMA treatment caused cell death in CA1, which was more extensive in the chronic treatment group.

Chronic exposure to lead (Pb) affects neural functions in central nervous system (CNS) particularly the learning and memory. On the other hand, alteration of calcium level in the CNS results in activation of NOS. It has been shown that lead enters the neurons through calcium channels and displaces Ca2+ from calcium binding proteins such as calmodulin and troponin C thereby affecting calcium-mediated processes.Our recently data showed that no prodaction due to NMDA receptor simulation in cultured CA1 PYRAMIDAL CELLS has been diminished in the presence of 10 nM of Lead acetate. Therefore, it is possible that Lead can inhibit the elevation of NO through blockade of NMDA receptor and interference of LTP through this mechanism. This finding may attribute to the effect of lead on the NOS activity or expression as key enzyme producing NO. In this study we have examined the effect of lead acetate on the NOS expression in the presence of NMDA agonist using immunocytochemical analysis. Expression of nNOS was examined in the CA1 PYRAMIDAL CELLS exposed to 10 and 100 nM lead acetate and 40 mM ACBD (NMDA agonist). The result of this experiment showed that the enhanced nNOS expression induced by ACBD significantly diminished by lead acetate. The trend of this inhibition is similar to amount of NO production indicating that the decrease of expression may major reason of decrease in NO production.

Since branching region of an active nerve fiber is an abrupt widening of the structure, two concepts emerge: first, the stimulating current must be sufficient to raise the outgrowing fibers above the thresh­old, and secondly, the stimulating current will be divided in proportion to the characteristic admittance of the branches. On the other hand, blocking of the nerve impulse in this region is an important issue that has been evaluated in several different ways including Hodgkin-Huxely, Markin-Chizmadzhev, general leading edge, cubic leading edge, and piecewise linear leading edge models. Each of these models has its advantages and disadvantages, but none of them can be completely accounted. Meanwhile, hippocampus is a part of the nervous system that is involved in sophisticated functions including memory. Hence, we have evaluated the behavior of branching dendrites in PYRAMIDAL CELLS of the hippocampus not only to elucidate the effect of branching on signal processing, but also to understand more precisely the function of PYRAMIDAL CELLS. In this study, MATLAB software (6.5) was used to design a program that evaluates the effect of branching point on propagation or blockade of impulse. In order to execute this program, we have modeled the nerve fiber as an electrical circuit and exerted some neurobiological features of PYRAMIDAL cell to this model. Finally, a MATLAB program was introduced that can be used as a model of PYRAMIDAL CELLS in experimental researches.

Background: Brain ischemia is one of the most important problems in the world and causes severe brain damages, especially in CA1 region of hippocampus. Calcium channel blockers, such as verapamil, have neuroprotective effects. This study was done to investigate neuroprotective effects of verapamil on the CA1 region of hippocampus in the male rat.Materials and methods: This experimental study was conducted on 24 male adult Wistar male rats (250-300 g) that were divided into four groups: control, ischemia, vehicle and treatment. For induction of ischemia, both common carotid arteries were blocked for 20 minute followed by reperfusion. Verapamil (10 mg/kg) was administrated 1 hour before and after ischemia intraperitoneally in treatment group. The brains were dissected and processed for Nissl staining. The results were analyzed by analysis of variance (ANOVA) and Tukey’s tests.Results: Data showed no significant difference between the number of viable PYRAMIDAL CELLS in CA1 region of hippocampus in control and 10 mg/kg verapamil treated groups, but number of PYRAMIDAL CELLS reduced in ischemia and vehicle groups and there was significant difference between these groups with control (P<0.05). This study showed that the injection 10mg/kg of verapamil can reduce damaged CELLS in CA1 region of hippocampus in rats that were subjected to transient global cerebral ischemia.Conclusion: It seems that administration of verapamil (10mg/kg) decreases severity of neuronal damage in CA1 CELLS of hippocampus in rat following transient ischemia reperfusion.

Background and Objectives: The increase of stress following technology development appears to be a threat to human body organs such as nervous system. The present study was conducted aiming at investigating the effects of chronic multiple stress on morphometric changes of Betz CELLS in male rat cerebral cortex.Methods: In this experimental study, 18 Wistar rats were randomly divided into two equal groups. Animals of the under stress group for 10 days were exposed to different stresses, such as food deprivation, water deprivation, forced swimming, immobilization at 4oC, and isolation, while the animals in control group were kept in their cages without any intervention. After the intended period, the animals were anesthetized and then their brains were removed. After fixation, samples of frontal cortex of the brain were prepared for light microscopy study. The data analysis were performed using t-test, and the significance level was considered p<0.05.Results: The mean number and size of Betz CELLS in the stress groups was significantly lower compared to control group (p<0.001). The qualitative observations also showed chromatolysis of nissl bodies, nucleus condensation, and decrease of neural processes.Conclusion: The results of the present study showed that chronic multiple stress can have negative effects on the rat cortical internal PYRAMIDAL layer through reducing the size and number of Betz CELLS; however, more studies are needed to confirm the above results.

Background: Thyroid hormones are well known to be essential for normal development of the brain in human and animals. In particular, thyroid deficiency during the prenatal periods causes significant impairments of structural development and organization of the brain. Therefore in this study, the effects of maternal hypothyroidism on morph metrical changes of synaptic sites of PYRAMIDAL CELLS in the mouse brain was evaluated.Materials and Methods: This study was carried out on 24 balb/c mice. The animals were divided into two experimental and control groups. The experimental group was made hypothyroid by chemical thyroidectomy with oral propylthyouracil (PTU) in drinking water, while the control group was kept intact. On the 20th postnatal day, by using histological technique preparation and histochemical staining (Golgy) method, we were able to investigate the effects of maternal thyroid hormones deficiency, on the development of PYRAMIDAL synaptogenesis in postnatal period of the mouse. Results: Our findings showed that maternal hypothyroidism during pregnancy cansed a significant decrease of the dendritic spines in the experimental group (31.08±0.45) compared with the control group (39.88±0.55), (p<0.05). In addition, an increase gap among the synaptic sites of PYRAMIDAL CELLS in the brain cortex among the experimental group (3.78±0.86) in contrast with the controls (2.57±1.05) were observed (p<0.005). Conclusion: The results of this study indicated that there is a key role for thyroid hormones in connection with maturation and neuronal development of brain cortex. Also hormonal reduction during pregnancy can affect the development and neuronal synaptogenesis of the next generation.

PYRAMIDAL CELLS of the dorsal cochlear nucleus (DCN) represent firing types with different latencies. They incorporate two transient potassium currents namely IKif and IKis with fast and slow inactivation gatings, respectively. Transient potassium currents i.e. currents having both activation and inactivation gatings influence on the latency before firing. These currents cause different neural responses containing a regular firing, or a long latency before firing with or without a leading spike. In this paper, the firing behavior of DCN PYRAMIDAL CELLS is simulated first with a 3-variable conductance-based model. Next, mechanisms underlie neural responses of the model are analyzed by dynamical systems analysis methods. The model is a reduced version of Kanold and Manis model with 10 variables.

Objective: Cerebral ischemic/reperfusion causes severe brain damage, especially in CA1 region of hippocampus. Nowadays, vasodilator drugs such as pentoxifylline are considered for their neuroprotective effects, but there is no study on possible neurotrophic effects of this drug and its effective dose on CA1 PYRAMIDAL CELLS of hippocampus in transient global ischemic/reperfusion on experimental models.Method: In this study male Wistar rats (n=30) in experimental groups 1, 2 and 3 were injected intraperitoneally by 200, 400 and 600 mg/kg pentoxifylline respectively one hour before and one hour after ischemia. Other groups were control, sham and vehicle (normal saline). Four days after ischemia, brains were removed and prepared for histological study (Nissl Method).Results: Our data showed that there was no significant difference between the number of viable PYRAMIDAL CELLS in CA1 region of hippocampus in control and 200 mg/kg pentoxifylline treated groups.Conclusion: It seems that the neuroprotective effect of 200 mg/kg pentoxifylline may be accompanied by a reduction of ischemic damage in CA1 region of hippocampus in rats that were subjected to transient global cerebral ischemia.

Background: Cerebral ischemia is known as a main cause of morbidity and mortality in the world and there was no effective treatment yet. Global cerebral ischemia causes loss of PYRAMIDAL CELLS of brain cortex following global ischemic/reperfusion. Recently, using immunophilin ligands has been considered as a potential and appropriate strategy for neuroprotection. Since it was observed that tacrolimus (FK506), a useful immunosuppressant used in organ transplantation, provides neuroprotection and prevents neuronal damage,the importance of immunophilins in the development of neuroprotectors has emerged. In this study, we investigated the neurotrophic effect of the immunosuppressant agent FK506 in rat after global cerebral ischemia.Materials and methods: In this experimental study, 25 Wistar rats were assigned to control (intact), ischemia and 3 FK506 treated (1, 3, 6 mg/kg) groups. Both common carotid arteries were occluded for 20 minutes followed by reperfusion. In 3 experimental groups, tacrolimus or FK506 was given as a single dose exactly at the time of reperfusion respectively as 1, 3, 6 mg/kg by intravenous administration (IV). The same doses repeated by intraperitoneally administration (IP) 48 hours after reperfusion. After 4 days, the rats were sacrificed and brain sections were stained by H & E and Nissl.Results: Our findings showed that 20 min ischemia decreased the number of the cortex PYRAMIDAL CELLS. But there were significant differences between number of cortex PYRAMIDAL CELLS in ischemia and FK506 (6mg/kg) groups.Conclusion: Our study suggests that tacrolimus has a neurotrophic effect on PYRAMIDAL CELLS of brain cortex and may candidate for treatment of ischemia brain damage.