Reciprocal trophic interactions in the adult climbing fibre-Purkinje cell system.

This article reviews a series of experiments aimed at investigating the reciprocal trophic interactions which regulate the normal morphofunctional features and the plasticity of the adult rodent climbing fibre-Purkinje cell system. Climbing fibre deprivation induces profound functional and structural changes in the Purkinje cell. Among others, proximal Purkinje cells dendrites become studded with numerous newly formed spines some of which are innervated by parallel fibres. These structural modifications are reversed if the Purkinje cell is reinnervated by another climbing fibre. These results indicate that the olivocerebellar input inhibits spinogenesis on proximal Purkinje cell dendrites and prevents other afferents from invading its own target domain. It is proposed that the normal distribution of synapses on the Purkinje cell dendritic tree is controlled by the interplay between climbing and parallel fibre influences on Purkinje cell dendrites. Following Purkinje cell death, the distal climbing fibre branches are withdrawn. This atrophy progresses according to the time and mode of Purkinje cell degeneration and it is reversed if the climbing fibre is provided with a new target Purkinje cell. In addition, sprouting from intact climbing fibres and collateral reinnervation of Purkinje cells can be obtained by both subtotal inferior olive lesions and transplantation of embryonic cerebellar tissue on the surface of the adult cerebellum. These results indicate that specific signals produced by non-innervated Purkinje cells are responsible for inducing and guiding climbing fibre sprouting. By contrast, contact cues would be necessary for the formation and the maintenance of terminal arbour branches and synapses. It is suggested that these interactions which control the structural plasticity following lesion or transplantation also operate during the fine structural remodelling underlying the functional plasticity in the intact cerebellar cortex.