Ca(2+)-activated potassium (K(Ca)) channel inhibition decreases neuronal activity-blood flow coupling

A number of possible mediators have been proposed to couple neuronal activity with local cerebral metabolic activity and blood flow, but the mechanisms by which these mediators act is still unclear. In order to explore these coupling mechanisms, we used the rodent whisker-barrel cortex (WBC) model to test the hypothesis that modulation of K(Ca) channels is an important step in this coupling process. Anesthetized rats were prepared for laser-Doppler flowmetry (LDF) or evoked potential recordings utilizing a thinned cranial window over WBC. Superfusion of the K(Ca) channel blockers tetraethylammonium (TEA) or iberiotoxin directly onto WBC attenuated the magnitude of the whisker evoked LDF changes. Similar effects were seen after intravenous administration of TEA. Although attenuated, neither the temporal profile of the elicited blood flow responses nor the evoked electrical activity in WBC were affected by K(Ca) blockade. These data suggest that the process of cerebral metabolism/blood flow coupling in the rodent WBC involves K(Ca) channels.