Dendritic Alterations of Cerebellar Purkinje Neurons in Postnatally Lead-Exposed Kittens

Abstract

Many investigations have sought to determine the effect of lead exposure on the development of the cerebellum. This study addresses the effects of postnatal lead exposure in kittens on dendritic development of Purkinje cells. Golgi-Cox filled cells were used to measure dendritic branching patterns, spine density, height, width and distance from the cerebellar surface. The results revealed a significant increase in spine density and altered patterns of dendritic branching. Complex dendritic branching was evident with a progressive shift in peak branching peripherally. Lead-exposed Purkinje cells showed early sprouting with subsequent pruning. At 5 weeks of age dendritic branches on experimental cells were increased along the entire dendritic extent. Control Purkinje cells showed initial sprouting with subsequent pruning. Normal developmental growth spurts and lead-induced effects were evident on dendritic height, width and distance from the surface. Cerebella stained with hematoxylin and eosin and cresyl violet acetate showed no evidence of vascular damage or other pathologies. These findings corroborate the evidence of hyperspiny dendritic formation representing an important mechanism of neuronal plasticity. In regard to morphological effects of lead on rodents, the hyperspiny Purkinje cell dendrites and patterns of dendritic growth in lead-treated kittens offer an alternative interpretation of neurobehavioral findings of lead-burdened children. The results are discussed with reference to other aspects of lead exposure and neural development.

Aging of cerebellar Purkinje cells

“…PCs are among the most vulnerable neurons in the brain (Patrick and Anderson 2000;Woodruff-Pak 2006;Servais et al 2007;Dhar et al 2007;Woodruff-Pak et al 2010) and are prone to aging insult (Quackenbush et al 1990;HadjSahraoui et al 2001;Andersen et al 2003;Zhang et al 2006). A complicated and disputed issue is whether the quantity of PCs decreases or remains constant during the normal aging process.…”

Gestational lead exposure induces developmental abnormalities and up-regulates apoptosis of fetal cerebellar cells in rats

“…It induces demyelination, reduces neuron populations, interferes with neurotransmission, decreases neuronal growth (Pearson & Schonfeld, 2003), and alters morphology of the developing cerebral cortex (Wilson et al, 2000). Changes in dendritic branching of cerebellar Purkinje cells have been proved to be associated with lead exposure in kittens (Patrick & Anderson, 2000). Lead exposure during embryonic development induces cortical and cerebellar damage in newborn rats (Gargouri et al, 2012), reduces neurogenesis in adult (Gilbert et al, 2005), and in the developing rat hippocampus (Chang et al, 2012).…”

Variations at a quantitative trait locus (QTL) affect development of behavior in lead-exposed Drosophila melanogaster

“…Chronic lead exposure decreases the density of dendritic spines and synapses in rats (Kiraly and Jones 1982; Petit and Alfano 1979; Petit and LeBoutillier 1979) and the number of synaptic contacts formed by retinotectal projections in frogs (Cline et al 1996) but increases dendritic spine density (presumably synaptic sites) on cortical pyramidal cells (Patrick and Anderson 1995) and cerebellar neurons (Patrick and Anderson 2000) in cats.…”