Purkinje cell spinogenesis during architectural rewiring in the mature cerebellum.
Spines can grow and retract within hours of activity perturbation. We investigated the time course of spine formation in a model of plasticity involving changes in brain architecture where spines of a dendritic domain become innervated by a different neuronal population. Following a lesion of rat olivocerebellar axons, by severing the inferior cerebellar peduncle, new spines grow on the deafferented proximal dendrite of the Purkinje cells (PCs) and these new spines become innervated by parallel fibres (PFs) that normally contact only the distal dendrites. The varicosities of climbing fibre (CF) terminal arbors disappear within 3 days of the lesion. Spine density in the proximal dendritic domain begins to rise within 3 days and continues to increase towards a plateau at 6-8 days. In 'slow Wallerian degeneration' mice, in which axonal degeneration is delayed, climbing fibre varicosities virtually disappear at 14 rather than 3 days. Spine density in the proximal dendritic domain is similar to control Purkinje cells up to 14 days and increases significantly 18 days postlesion. The delayed spinogenesis in the latter mutant is the result of a persistence of the climbing fibre presynaptic structure in the absence of activity. Therefore, climbing fibre activity itself is not directly responsible for the suppression of spine formation, but suppression mechanisms tend to become weaker as long as the structural dismantling of the presynaptic varicosities proceeds. Thus, spinogenesis is guided by two different mechanisms; a rapid one related to changes in homotypic remodeling and a slower one, which requires the removal of a competitive afferent.
Cesa
Roberta
R
Rita Levi Montalcini Center for Brain Repair, Department of Neuroscience, University of Turin, C.so Raffaello 30, 10125 Turin, Italy. roberta.cesa@unito.it
Morando
Laura
L
Strata
Piergiorgio
P
D000818:Animals; D064026:Calbindins; D002531:Cerebellum / Q000166:cytology* / Q000502:physiology; D003712:Dendrites / Q000502:physiology*; D049229:Dendritic Spines / Q000502:physiology* / Q000648:ultrastructure; D005455:Fluorescent Antibody Technique / Q000379:methods; D026901:Membrane Transport Proteins / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008818:Mice, Neurologic Mutants; D018613:Microscopy, Confocal / Q000379:methods; D008854:Microscopy, Electron / Q000379:methods; D009412:Nerve Fibers / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000172:deficiency; D009473:Neuronal Plasticity / Q000502:physiology; D009847:Olivary Nucleus / Q000293:injuries / Q000473:pathology / Q000648:ultrastructure; D011689:Purkinje Cells / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D017208:Rats, Wistar; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D013997:Time Factors; D050599:Vesicular Glutamate Transport Protein 2
D064026:Calbindins; D026901:Membrane Transport Proteins; D009419:Nerve Tissue Proteins; D064030:S100 Calcium Binding Protein G; C493477:Slc17a6 protein, mouse; C493475:Slc17a6 protein, rat; D050599:Vesicular Glutamate Transport Protein 2; C442580:Wld protein, mouse