Arteriole responses to mGluR agonist application are eliminated in cPLA₂α^−/− neocortical slices.

Abstract

<p><b>A.</b> Bath application of 1S,3R-ACPD 50 µM to slices equilibrated with 95% O₂ induced constriction of arterioles in cortical slices of cPLA₂α^+/+ (empty square, n = 29), but not cPLA₂α <b>⁻</b>^/− mice (filled square, n = 15). Washout of 1S,3R-ACPD was followed by application of 10 µM PGE₂ which caused identical constriction of arterioles in both genotypes. <b>B.</b> In slices at equilibrium with 95% O₂, arterioles were preconstricted with 100 nM U-46619 supplemented ACSF. To compare acute cPLA₂α inhibition with gene deletion, cPLA₂α^+/+ slices were treated with 10 µM ATK (filled black triangle, n = 21) for the duration of the experiment. Inset shows the complete experiment from the time of application of U-46619. The dashed white box indicates the expanded graph. After 30 min equilibration in U-46619, 1S,3R-ACPD was added to the bath at a final concentration of 50 µM (time  = 0) and the responses of arterioles in cPLA₂α^+/+ (n = 21) and cPLA₂α<b>⁻</b>^/− (n = 25) cortical slices were compared to cPLA₂α^+/+ slices that were not treated with 1S,3R-ACPD (red empty triangle, n = 10). *, <i>P</i><0.05; **, <i>P</i><0.01; ***, <i>P</i><0.001. <b>C.</b> When slices were equilibrated in 20% O₂, 1S,3R-ACPD treatment dilated cPLA₂α^+/+ (n = 18) but not cPLA₂α<b>⁻</b>^/− (n = 16) arterioles. Bath application of 10 µM PGE₂ caused dilation of both genotypes. ***, <i>P</i><0.001.</p