We investigated the contribution of ATP-sensitive potassium channels (K(ATP)) and calcium-activated potassium channels (K(ca2+)) to cortical spreading depression (CSD)-associated hyperemia using the rat closed cranial window model. The peak CBF response was enhanced by 12 ± 5, 13 ± 4, and 28 ± 8% (p < 0.01) of the control with 10-6, 10-5 and 10-4 mol/l glibenclamide (glyb), a K(ATP) antagonist, respectively. We also calculated the area under the CBF curve to fully represent the extent of hyperemia during CSD. The area increased by 30 ± 8 (p < 0.05), 72 ± 31 (p < 0.05) and 88 ± 20% (p < 0.05) of the control with 10-6, 10-5 and 10-4 mol/l glyb, respectively. However, charybdotoxin (CTX), a K(ca2+) antagonist showed no effect. The effect of glyb was inhibited by pretreatment with 5 mg/kg indomethacin. We conclude that activation of K(ATP) perhaps associated with neurons, plays an inhibitory role in the CSD-associated hyperemia via an indomethacin-sensitive mechanism. (C) 2000 Lippincott Williams and Wilkins.
- Cerebral blood flow
- Cortical spreading depression (CSD)
- Potassium channels
ASJC Scopus subject areas