Malformation of purkinje cell dendrites induced by graft-versus-host disease

W. S T Griffin, M. A E Eriksson, E. N. Crom, J. R. Head

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Impairment of cerebellar Purkinje cell growth was assessed in Golgi-Cox stained tissue in 14 day old (Fischer X DA)F1 hybrid rats subjected to graft versus host disease (GVHD). GVHD was induced by grafting parental strain lymph node cells (PSLNC) into the anterior facial vein on the day of birth. We have previously described GVHD induced changes in nucleotide and protein content [12] and RNA function [14] as well as alterations in cell numbers and areas of the external granular and molecular layers in diseased animals [13]. In this report some effects of GVHD on the gross morphology of Purkinje cells in 14 day old animals are enumerated. Most Purkinje cells (62%) from GVHD animals had a height to width ratio greater than 1, whereas most from control animals (71%) had ratios of less than 1. The majority of Purkinje cells (67%) from diseased animals had elongated main dendrites which were devoid of branches and often (13%) these elongated main dendrites were S-shaped. In addition, comparison of Purkinje cells from GVHD and control animals revealed a greater tendency (15%) toward retention of extrasomal processes in GVHD animals. These findings suggest that GVHD affects nondividing, differentiating cell populations as well as those which are proliferating and migrating. Our evidence that, as a result of GVHD, the protein synthesizing capacity of the cerebellum is altered [14] and that Purkinje cells are more closely spaced at day 11 suggests that both intrinsic and extrinsic factors are involved in producing the changes in dendritic shape reported here.

Original languageEnglish (US)
Pages (from-to)673-678
Number of pages6
JournalBrain Research Bulletin
Volume5
Issue number6
DOIs
StatePublished - 1980

Keywords

  • Graft-versus-host disease
  • Purkinje cell malformation

ASJC Scopus subject areas

  • General Neuroscience

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