Relative CBF was continuously monitored at the site of the cranial window using a laser-Doppler probe (Moor Instruments; Axminster, UK) positioned stereotaxically 0.5 to 1 mm from the cortical surface. CBF values were expressed as percent increase relative to the resting level [(CBFstimulus–CBFresting)/CBFresting]. Zero values for CBF were obtained after the heart was stopped by an overdose of isoflurane at the end of the experiment (Capone et al., 2012 (link)).
CBF recordings were started after arterial pressure and blood gases had reached a steady state, as previously described (Capone et al., 2012 (link)). All pharmacological agents and drugs studied were dissolved in a modified Ringer’s solution (Girouard et al., 2006 (link)). The increase in CBF produced by somatosensory activation was assessed by stimulating the whiskers contralateral to the cranial window by side-to-side deflection for 60 s. The endothelium-dependent vasodilator acetylcholine (10 µmol/L; Sigma-Aldrich) was topically superfused for 5 min, and the resulting changes in CBF were monitored. CBF responses to the smooth muscle-dependent relaxant adenosine (400 µM; Sigma-Aldrich) were also examined.
CBF recordings were started after arterial pressure and blood gases had reached a steady state, as previously described (Capone et al., 2012 (link)). All pharmacological agents and drugs studied were dissolved in a modified Ringer’s solution (Girouard et al., 2006 (link)). The increase in CBF produced by somatosensory activation was assessed by stimulating the whiskers contralateral to the cranial window by side-to-side deflection for 60 s. The endothelium-dependent vasodilator acetylcholine (10 µmol/L; Sigma-Aldrich) was topically superfused for 5 min, and the resulting changes in CBF were monitored. CBF responses to the smooth muscle-dependent relaxant adenosine (400 µM; Sigma-Aldrich) were also examined.
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