The plasticity of the Purkinje cell.
Dendritic plasticity in man is analysed on the example of the Purkinje cell. The conspicuous and easily demonstrable dendrites of this cell lend themselves particularly to such a study. Abnormalities of the dendritic tree have been observed in a variety of conditions, some of them originating in early infancy, others acquired in later life, all of them associated with a substantial loss of granule cells. While differences between the various diseases undoubtedly exist, the basic pattern remains remarkably constant. Three types of dendritic abnormality may be present: (i) persistence or neoformation of somal dendrites; (ii) expansion and malorientation of primary apical dendrites (the staghorn deformity); and (iii) bizarre ramification of secondary and tertiary dendrites, sometimes associated with expansions known as cactus, stellate or sunray figures. It is suggested that all these features should be interpreted as a response of the Purkinje cell to partial deafferentation and not as congenital malformations. In addition, dislocation of the Purkinje cell into the molecular layer is frequently seen in this group of cases. This may be ascribed to loss of tethering of the cell by its afferent fibres.
D000328:Adult; D000818:Animals; D001284:Atrophy; D001927:Brain Diseases / Q000473:pathology*; D002524:Cerebellar Ataxia / Q000473:pathology; D002526:Cerebellar Diseases / Q000473:pathology; D003712:Dendrites; D006801:Humans; D007223:Infant; D008297:Male; D007706:Menkes Kinky Hair Syndrome / Q000473:pathology; D008630:Mercury Poisoning / Q000473:pathology; D051379:Mice; D009472:Neuronal Ceroid-Lipofuscinoses / Q000473:pathology; D009473:Neuronal Plasticity; D011689:Purkinje Cells / Q000473:pathology*