Transient occlusion of rat carotid arteries increases formation of inositol phosphate. Evidence for a specific effect on α₁-receptors

Rats which had both carotid arteries occluded (BCCA) for 24 min did not suffer histological damage to hippocampal tissue. However, BCCA treatment followed by transient normobaric hypoxia (reduced oxygen) for 30 min caused damage to the pyrimidal cells in the hippocampus. Intraventricular injection of [³H]inositol followed by BCCA + hypoxia treatment caused an increase in the release of [³H]inositol-mono-phosphate ([³H]Ins-1-P) and [³H]inositol-bis-phosphate ([³H]Ins-2-P) in both groups (BCCA and BCCA + hypoxia) but not in sham controls. These results suggest that BCCA or oxygen reduction stimulates phosphoinositide metabolism, causing a release of [³H]inositol triphosphate ([³H]Ins-3-P). Agonist-induced stimulation of inositol phosphates (InsPs) was also analysed in BCCA animals 3 and 14 days after their operations. Noradrenaline produced an increase in Ins-Ps in the hippocampus (but not in the frontal cortex) 14 days after BCCA. This effect did not occur for sham controls nor for carbachol and quisqualate stimulation. The results show a delayed effect of the α₁-receptors in the hippocampus of BCCA animals.