Abstract
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 were examined in the CA1 pyramidal cells exposed to 10 and 100 nM lead acetate and 40 µM 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.
Keywords
Expression nNOS Pyramidal cell NMDA agonist ACBD Lead acetate
Copyright
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