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.

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.

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.

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.

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.