ATP sensitive K+ channels (K-ATP) of glucose sensing pancreatic β cells regulate insulin secretion. Elevation of intracellular ATP closes K-ATP which depolarizes the cell and increases intracellular Ca++ which then mediates insulin secretion. Moreover, slow oscillations of K-ATP activity (in the presence and absence of glucose) correspond to oscillations of intracellular Ca++ concentration that are synchronized to pulsatile insulin release. These K-ATP channels are also located on glucose sensing neurons of hypothalamic regions associated with autonomie regulation. Thus, these neurons may provide a mechanism whereby metabolic status influences autonomie activity. We investigated the properties of K-ATP in the VMN with cell attached and inside-out patch clamp recording for neurons isolated from neonatal rats. Cells were incubated in glucose free medium for 30 min prior to recording to maximize the probability of K-ATP opening (P0). Although we identified channels that appeared to be inhibited by glucose and ATP, consistent results were difficult to obtain due to large fluctuations in P0. That these fluctuations were observed in both cell attached and inside out preparations is consistent with the fluctuations occurring in the βcell both in the presence and absence of glucose. We hypothesize that these fluctuations are an intrinsic property of the K-ATP channel in the VMN.
|Original language||English (US)|
|State||Published - Dec 1 1996|
All Science Journal Classification (ASJC) codes
- Molecular Biology