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The effects of intrauterine growth retardation on the development of the Purkinje cell dendritic tree in the cerebellar cortex of fetal sheep: A note on the ontogeny of the Purkinje cell
Author(s) -
Rees Sandra,
Harding Richard
Publication year - 1988
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(88)90052-4
Subject(s) - purkinje cell , cerebellum , biology , cerebellar cortex , dendritic spine , granule cell , fetus , golgi apparatus , anatomy , nissl body , neuroscience , cell , central nervous system , pregnancy , biochemistry , staining , dentate gyrus , genetics , hippocampal formation
The development of the fetal sheep cerebellum at 80, 100, 120 and 140 days gestation (term = 146 days) and 3 months postnatally was studied using Nissl stained sections and rapid Golgi preparations. The most rapid expansion of the Purkinje cell dendritic tree occurred between 100 and 120 days of gestation (5–6 fold increase in area). By 140 days it had acquired its adult form after which time growth continued mainly in the vertical direction. The effects of intrauterine growth retardation on the growth of granule and Purkinje cell dendrites in the cerebellar cortex of fetal sheep (140 days) were investigated in Golgi preparations. Compared with control cerebella the length (but not the number) of granule cell dendrites was reduced by 14% ( P <0.01); the area of the Purkinje cell dendritic field was reduced by 20% ( P <0.01); the branching density was reduced by 8% ( P <0.01); the total branch length was reduced by 27% ( P <0.002); the density of dendritic spines per row was not affected. These factors resulted in a decrease of 26% ( P <0.002) in the total number of dendritic spines per row per Purkinje cell. These findings show that the growth of granule cell dendrites and the Purkinje cell dendritic tree have been significantly affected by chronic intrauterine deprivation. Such structural abnormalities could affect the pattern of neuronal connectivity and could be associated with functional deficits.