Alteration of opioid peptide and receptor ontogeny in the brain of pre- and postnatally low-level lead-exposed rats.

While the dopaminergic, the cholinergic and the GABAergic systems have been extensively studied in various models of lead intoxication, less attention has been devoted to the brain opiatergic system (opioid). We have recently reported that in rats pre- and postnatally exposed to a very low amount of lead (1 mg/kg/day) there was, at 40 days of age (behavioural anomalies such as hypermotility and decreased response to pain stimuli), an increased number of opiate receptors in the brain associated to a decrease of beta-endorphin and an increase of Met-enkephalin. The aim of the present study was to find out whether the above mentioned abnormalities of the opiatergic system (opioid) could be the result of a neurotoxic effect of lead exerted early in the development of the central nervous system of rats born from lead-poisoned parents. Here we report that the exposure to a low level of lead induces a decrease of beta-endorphin with a concomitant increase of opiate receptors measured at embryonic day 16 as well as at 7, 15, 40 and 60 days postnatally. On the other hand, an increased presence of Met-enkephalin was not detectable until postnatal day 7. Since endogenous opioid peptides, particularly beta-endorphin, have been recognized as important factors in central nervous system development, the described ability of lead to affect the ontogeny of the opiatergic system (opioid) might provide a new insight in understanding the complex mechanism of lead neurotoxicity.