The pattern of ATP-sensitive K+ channel subunits, Kir6.2 and SUR1 mRNA expressions in DG region is different from those in CA1-3 regions of chronic epilepsy induced by picrotoxin in rats.

ATP-sensitive K(+) (K(ATP)) channel's function is a key determinant of both excitability and viability of neurons. In the present report, in situ hybridization histochemistry and Western blot were used to examine whether picrotoxin (PTX)-kindling convulsions involved the changes in distribution of K(ATP) channels. The data demonstrated that the formation of kindling state was associated with a decreased amount of Kir6.2 mRNAs and proteins both in cerebral cortex and dentate gyrus (DG) as well as with a decreased amount of (regulatory subunit) SUR 1 mRNAs in DG. In contrast, resulting from a PTX re-induced seizure insult, both subunits were transiently up-modulated but not exactly paralleled between them and among different regions. In DG, Kir6.2 mRNAs increased toward normal levels at 12 h, followed a gradual decrease from 1 day to 3 days, being distinct from that detected in CA1-3 regions in which no significant change was shown. Further, SUR1 mRNAs markedly increased at 12 h, decreased significantly at 1 day, and even went down to a faint level at 3 days which was similar to that of CA1-3 regions, and there was no significant change in CA1-3 regions of SUR1 mRNAs. Also, at 7 days after a PTX re-treatment, Kir6.2 proteins increased significantly in the cortex, CA1, CA3 and DG (increasing 49.52%, 39.36%, 33.41%, and 54.79%, respectively) as well, SUR1 proteins increased significantly in DG (increasing 3.42 times), as compared with kindling rats without PTX retreatments (P < 0.05). These results indicated that K(ATP) channels in brain particularly in DG are likely related to enhanced seizure susceptibility and dynamic controls of seizure propagation of chronic epilepsy induced by PTX in rats.