Ogundele, O.M and Madukwe, J
Cyanide is a potent neurotoxin capable of potentiat ion NMDA R1 (N-methyl-D-aspartate Receptor 1) a form of glutamate receptor that is calcium gated, t hus causing excitotoxicity. It is also well establi shed that the glutamate-glucose exchange is dependent on the activity of the Na + /K + ATPase pump, thus we examine the role of the Na + /K + pump in the metabolism of the neuron during cyanid e toxicity. Six separate perfusion set up of the rat brain cortical tissues were made with ACSF (Accessory cerebrospinal fluid) (ACSF, ACSF+KCN (potassium cya nide), ACSF+KCN + pump blocker, ACSF + pump blocker). The tissues were perfused for duration of 180 minutes. The tissues were processed histologically to study the membrane and axonal str ucture. The pump blockers (methyldigoxin and promethazine) induced excitotoxicity when used in c ulture, and amplified cyanide toxicity when combined with KCN. Cell enlargement was characteri stic of both cyanide and pump blocker treated cultures, the pattern of cell enlargement observed in the methyldigoxin/promethazine treated tissues shows more of osmotic imbalance induced cell enlarg ement while the Cyanide treated sections showed moderate enlargement as osmotic imbalance is believ ed to be a latter event is this tissue.
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