The effects of changes in membrane cholesterol on ion currents were investigated in pituitary GH 3 cells. Depletion of membrane cholesterol by exposing cells to methyl-β-cyclodextrin (MβCD), an oligosaccharide, resulted in an increase in the density of Ca 2+ -activated K + current (I K(Ca) ). However, no significant change in I K(Ca) density was demonstrated in GH 3 cells treated with a mixture of MβCD and cholesterol. Cholesterol depletion with MβCD (1.5 mg/ml) slightly suppressed the density of voltage-dependent L-type Ca 2+ current. In inside-out patches recorded from MβCD-treated cells, the activity of large-conductance Ca 2+ -activated K + (BK Ca ) channels was enhanced with no change in single-channel conductance. In MβCD-treated cells, voltage-sensitivity of BK Ca channels was increased; however, no change in Ca 2+ -sensitivity could be demonstrated. A negative correlation between adjacent closed and open times in BK Ca channels was observed in MβCD-treated cells. In inside-out patches from MβCD-treated cells, dexamethasone (30 μM) applied to the intracellular surface did not increase BK Ca -channel activity, although caffeic acid phenethyl ester and cilostazol still opened its probability effectively. However, no modification in the activity of ATP-sensitive K + channels could be seen in MβCD-treated cells. Current-clamp recordings demonstrated that the cholesterol depletion maneuver with MβCD reduced the firing of action potentials. Therefore, the increase in BK Ca -channel activity induced by membrane depletion may influence the functional activities of neurons or neuroendocrine cells if similar results occur in vivo.
|Number of pages||13|
|Journal||Chinese Journal of Physiology|
|Publication status||Published - 2006 Jan 1|
All Science Journal Classification (ASJC) codes
- Physiology (medical)