PYRITINOL FACILITATES THE RECOVERY OF CORTICAL CHOLINERGIC DEFICITS CAUSED BY NUCLEUS BASALIS LESIONS

The effect of a nootropic, Pyritinol, on the recovery of cortical chol inergic deficits induced by injury of the nucleus basalis has been tes ted on two groups of unilateral quisqualic acid nbM-lesioned rats. The first group had a 30 nmol lesion producing a cortical cholinergic imp airment at 21 days, with a spontaneous recovery at 45 days. The second group had a 50 nmol lesion that produced a deeper cholinergic deficit , which did not recover at 45 days. Pyritinol enhanced the recovery in the 30 nmol group of animals on the 21st day after surgery. The recov ery was measured as an increase in the activities of acetylcholinester ase (AChE), choline acetyltransferase (ChAT) and the high affinity cho line uptake system, and the histochemical densities of the cortical AC hE network and the M(2) receptor. Histochemical analysis of the nbM en abled cortical recovery to be related to the number of surviving neuro ns and also to their hypertrophy and AChE-ChAT hyperactivity. Pyritino l enhanced recovery in 30 nmol lesioned animals but in the other group , with a lower number of surviving neurons and a lower ability of the cells to become hypertrophic, the drug was unable to promote cortical recovery.