Cholinergic depletion by IgG192-saporin retards development of rat barrel cortex

This study examines the role of cholinergic projections from the basal forebrain on development of the rodent barrel cortex. Pups were administered the immunotoxin IgG192-saporin (0.1 microg) intraventricularly at postnatal day (P) 0 and sacrificed at P1-P7. One ventricle was injected with saporin while the other side received saline, allowing comparison between the two sides of the same animal, as well as with controls receiving saline only. Compared to control animals, neuronal loss in the basal forebrain was present on both sides of saporin-treated pups but was significantly greater on the toxin-treated side, in all age groups and regions sampled. Depletion of acetylcholine did not prevent the formation of the barrel pattern, however it delayed its emergence by approximately 1 day. At P4, the thickness of layer IV barrel cortex was also significantly reduced; this reduction was undetectable by P7. From P3 to P5, the ratios of intensity of staining for acetylcholinesterase between the barrel centres and septa on the toxin-treated side were significantly lower than those on the saline side, although normal densities were present by P7. Thus, the depletion of cholinergic innervation at birth causes a transient delay in the development of the barrel pattern during the first postnatal week.