Background:

BMS 191011 is a maxi-K channel opener [1].

Maxi-K channels consist of a pore-forming α subunit and a regulatory β subunit. Maxi-K channels are of a high Ca2+ sensitivity [2].

Bath application of BMS-191011 at a concentration of 20 μM strongly reduced the calcium transients. This effect was associated with bursts of bAPs (100 Hz) recorded from Fmr1-/y dendrites without affecting those recorded from wild-type dendrites. This treatment decreased dendritic calcium transients of Fmr1-/y neurons to baseline levels of wild-type neurons [3]. In normoxia, BMS-191011 significantly induced cell death. This effect was indicted by the increases in propidium iodide (PI) uptake by 9.4 ± 2.4 and 16.8 ± 2.1% at 12 and 24 h treatments, respectively. At 12 h and then 24 h, the cellular [ATP] was decreased to 83.4 ± 3.1 and further to 72.3 ± 2.8%. During hypoxia, these effects were increased by