01 September 1997
Med Sci Monit 1997; 3(5): BR631-636 :: ID: 501511
Aluminium (Al) is known to cause neurotoxic effects and neurological disorders, as well as damage to peripheral tissues. Previously we showed that long-term exposure to Al induced damage of the central dopamine system in rats. This study was designed to determine whether reactivity of other central neurotransmitter systems, such as cholinergic and serotoninergic, might be altered by ontogenetic administration of Al. Aluminium sulfate (600 or 3000 ppm) was added to the drinking water of pregnant Wistar rats, starting from the first day of pregnancy and continuing until the day of weaning. Another group of rats was given Al in the same amount, 6 weeks to six months of age. Control groups consumed acidified water. At the age of 6 months all rats were injected with either mCPP (a central 5-HT2, receptor agonist) or pilocarpine (a muscarinic receptor agonist) and specific behavior (oral activity) was evaluated quantitatively. Prenatal exposure with Al did not changed muscarinic receptors reactivity to pilocarpine, but increased reactivity of the 5-HT2C, receptors to mCPP in 6 month old offspring. Long-term postnatal exposure with Al for 4.5 month diminished reactivity of the central muscarinic and 5-HT2C, receptor reactivity to specific agonists in 6 month old rats. These findings indicate that Al alters sensitivity status of 5-HT2C, receptors in rats, and the direction of change is dependent on the stage of development at the time of exposure.
Keywords: aluminium, serotonin receptors, muscarine receptors, m-chlorphenylpiperazine, Pilocarpine
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