Effects of Aβ1–42 on the Subunits of KATP Expression in Cultured Primary Rat Basal Forebrain Neurons

ATP-sensitive potassium channels (K ATP ) play a crucial role in coupling metabolic energy to the membrane potential of cells, thereby functioning as cellular “metabolic sensors.” Recent evidence has showed a connection between the amyloid neurotoxic cascade and metabolic impairment. With regard to their neuroprotection in other neuronal preparations, K ATP channels may mediate a potential neuroprotective role in Alzheimer’s disease (AD). To investigate the effects of Aβ 1–42 on the subunits of K ATP expression in cultured primary rat basal forebrain cholinergic neurons, primary rat basal forebrain neurons were cultured and evaluated. The subunits of K ATP : Kir6.1, Kir6.2, SUR1 and SUR2 expressing changes were observed by double immunofluorescence and immunoblotting when the neurons were exposed to Aβ 1–42 (2 μM) for different time (0, 24, 72 h). We found a significant increase in the expression of Kir6.1 and SUR2 in the cultured neurons being exposed to Aβ 1–42 for 24 h, while Kir6.2 and SUR1 showed no significant change. However, after being treated with Aβ 1–42 for 72 h, the expression of the four subunits was all increased significantly compared with the control. These findings suggest that being exposed to Aβ 1–42 for different time (24 and 72 h) induces differential regulations of K ATP subunits expression in cultured primary rat basal forebrain cholinergic neurons. The change in composition of K ATP may contribute to resist the toxicity of Aβ 1–42.