The effect of low level lead exposure on the postnatal structuring of the rat cerebellum

δ-Aminolevulinic Acid Dehydratase Activity in Weanling and Adult Rats Exposed to Lead Acetate

“…On the other hand, there were no changes in forebrain-to-body-weight ratio or cerebellum-to-body weight ratio in any lead-exposed group. This is in accordance with literature which reports no overt anatomical changes in cerebral tissues associated with low-level lead exposure in offspring (Hasan et al 1989, Rocha et al 1995.…”

Neuroteratological Consequences of Chronic Low-Level Lead Exposure

“…The details of this procedure have been described previously [24], Animals which were transiently exposed to low-level lead from time of conception to postnatal day 30 had difficulty in acquiring the task, whereas those exposed from time of birth to postnatal day 30 could acquire the task but had an impaired consolidation pro cess as judged by the pronounced decay in recall ability (table 1). These increased stepdown latencies cannot be attributed to leadinduced hyperactivity, as open-field studies and a subsequent increase to approximately 45 pg/dl on postnatal day 20 when the pups become mobile and have direct access to the drinking water [5], A similar developmental pattern in pup blood lead level is obtained with exposure to either 200 or 400 mg PbCVl drinking water from time of birth, but the early perinatal peak is absent ( fig. 3).…”

“…Delays in cell acquisition and positioning and fibre elabo ration could result in a retarded desialylation of embryonic NCAM, however, there is little evidence for this suggestion. Although lead lengthens the neural-cell cycle in a non specific manner, it does not appear to impair cell acquisition during the postnatal struc turing of the cerebellum [5,25], Further, lead has no effect on fibre outgrowth from spinal-cord expiants cultured on collagen matrices [26]. However, lead has been dem onstrated to have an effect on glial pheno type both in vivo and in vitro.…”

“…In vivo chronic low-level lead preco ciously induces the developmental increase in glial-specific glutamine synthetase [26]. These observations may reflect a precocious state of glial differentiation and, if cell sur face phenotype is similarly altered, the po tential to impair neuronal-cell movement along the radial processes formed by astro cytes [27], However, chronic low-level lead exposure does not impair the movement of the granule-cell perikarya on the Bergmann glia during their transit from the external to internal layer in the postnatal structuring of the cerebellum [5], Thus the lead-impaired E-to-A conversion of NCAM cannot be asso ciated with a developmental delay or gross structural alteration. Chronic low-level lead has been demon strated to significantly reduce the number of phosphotungstic acid-stained cortical synap ses on postnatal day 15 [8].…”

“…1,2], Cross-fostering studies suggest that lead mediates its action on the neurodevelopmental processes associated with the early perinatal period [3,4], How ever, low-level lead (20-40 pg/dl blood) does not induce gross abnormalities in the postna tal structuring of the cerebellum in which the entire neurodevelopmental process is en compassed [5]. Given that low-level lead im pairs cognitive and behavioural functions, it is not unreasonable to assume that this may teins which are the products of a single gene [9] .…”