title: Neonatal electrolytic lesions of the basal forebrain stunt plasticity in mouse barrel field cortex.
abstract: Previous studies have shown that neonatal electrolytic lesions of basal forebrain cholinergic projections in mice lead to a transient cholinergic depletion of neocortex and to permanent alterations in cortical cytoarchitecture and in cognitive performance. The present study examines whether neonatal electrolytic lesions of the basal forebrain modify neocortical plasticity. Using cytochrome oxidase histochemistry, we compared cross-sectional areas of individual barrels in the barrel field of four groups of postnatal day 8 (P8) old mice that on P1 received either (1) right electrolytic lesions of the basal forebrain, (2) left C row 1-4 whisker follicle ablations, (3) combined lesion treatments or (4) ice anesthesia only. The size of barrels in basal forebrain lesioned animals was not significantly different from controls. However, the plastic response to whisker removal was compromised in basal forebrain lesioned animals. An index of plasticity, the ratio of row D/row C areas, was reduced significantly in the combined nBM lesioned/follicle ablation group. Compared to whisker-lesioned mice, the expansion in rows B and D and the shrinkage in the lesioned row C area were diminished in the combined treatment group. The present findings correspond to those from a study of rats injected with a cholinergic immunotoxin [Cereb. Cortex 8 (1998) 63]. These results suggest that cholinergic inputs play a role in regulating plasticity as well as in the morphogenesis of mouse sensory-motor cortex.
authors.affiliation: Neuroscience Laboratory, The Kennedy Krieger Research Institute, 707 North Broadway, Baltimore, MD 21205, USA.
authors.forename: Akira
authors.initials: A
authors.lastname: Nishimura
authors.forename: Christine F
authors.initials: CF
authors.lastname: Hohmann
authors.forename: Michael V
authors.initials: MV
authors.lastname: Johnston
authors.forename: Mary E
authors.initials: ME
authors.lastname: Blue
mesh_terms: D000109:Acetylcholine / Q000172:deficiency*; D000110:Acetylcholinesterase; D000344:Afferent Pathways / Q000166:cytology / Q000254:growth & development / Q000502:physiology; D000375:Aging / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure; D020532:Basal Nucleus of Meynert / Q000166:cytology / Q000254:growth & development* / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology; D002799:Cholinergic Fibers / Q000502:physiology* / Q000648:ultrastructure; D051379:Mice; D008807:Mice, Inbred BALB C; D009434:Neural Pathways / Q000166:cytology / Q000254:growth & development* / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D013003:Somatosensory Cortex / Q000166:cytology / Q000254:growth & development* / Q000502:physiology; D014738:Vibrissae / Q000293:injuries / Q000294:innervation
chemical_list: D000110:Acetylcholinesterase; D000109:Acetylcholine