Cortical muscarinic receptor function following quinolinic acid-induced lesion of the nucleus basalis magnocellularis.

Phosphatidylinositol metabolism, linked to muscarinic receptor activation, was studied in rat cortical slices after a unilateral quinolinic acid lesion to the nucleus basalis magnocellularis (nbM) or the cortex itself. The incorporation of [3H]inositol into inositol phosphate was measured in the presence of LiCl, followed by anion exchange chromatography to separate inositol phosphates. Carbachol produced a dose-related increase in the amount of inositol phosphate in both the control and the cortex from rats with lesions to the nbM. No significant difference in the accumulation of inositol phosphate was observed between the two groups. Destruction of cortical cells with quinolinic acid almost completely eliminated the activation of phosphatidylinositol metabolism by carbachol. These results suggest that muscarinic receptors linked to phosphatidylinositol metabolism in the cortex are localized on intrinsic cortical neurons and not on afferent terminals from basal forebrain cholinergic neurons.