چكيده لاتين :
Chronic exposure to lead (Pb) affects neural function s 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 displa ces 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 ofNO through blockade ofNMDA receptor and
interference of LTP through this mechani sm. This finding may attribute to the effect of lead on
the NOS activi ty 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 agon ist using
immunocytochemical analysis. Expression of nNOS were examined in the CA1 pyramidal
cells exposed to 10 and 100 nM lead acetate and 40 fLM ACBD (NMDA agoni st). 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 ofNO production
indicating that the decrease of expre ssion may major reason of decrease in NO production.
