Chloride dysregulation delays post-awakening recovery

This proposed mechanism asks why awakening recovery may stay disrupted despite menopause-related hot-flash suppression. In an ovarian-withdrawal model, repeated awakenings could alter how hypothalamic stress-output neurons, brain cells governing stress signals, respond to gamma-aminobutyric acid, an inhibitory brain signal. Chloride inside them may turn that signal electrically activating, delaying sleep re-entry and the settling of heart rate and blood pressure. The test verifies hot-flash suppression under neurokinin 3 receptor blockade, then checks that KCC2, a transporter moving chloride out of these neurons, restores inhibition. Normal recovery with flashes suppressed would support the chloride mechanism; failure would retain rival explanations.