Perinatal exposure to polychlorinated biphenyls Aroclor 1016 or 1254 did not alter brain catecholamines nor delayed alternation performance in Long-Evans rats

Several reports have indicated that polychlorinated biphenyls (PCB) altered development of biogenic amine systems in the brain, impaired behavioral pe rformances, and disrupted maturation of the thyroid axis. The current study examines whether these developmental effects of PCB are correlated. Timed- pregnant Long-Evans rats were gavaged with the PCB mixture Aroclor 1016 (A- 1016, 10 mg/kg)from gestation day (GD) 6 to parturition. Some pups continue d to receive daily oral administration of PCB (10 mg/kg) until weaning at p ostnatal day (PD) 21. Another group of pregnant rats was given Aroclor 1254 (A-1254, 8 mg/kg) daily from GD 6 to weaning. At various age intervals, ra ts were sacrificed and six brain regions (prefrontal cortex, striatum hippo campus, diencephalon, cerebellum, midbrain + brain stem) were removed and a nalyzed for dopamine (DA) and norepinephrine (NE) levels by high-performanc e liquid chromatography. In addition, transmitter turnover rates were deter mined after an acute treatment of a-methyl-p-tyrosine. Serum samples were c ollected and analyzed for triiodothyronine (T-3) and thyroxine (T-4) by rad ioimmunoassay. Behaviorally, rats were evaluated for spatial learning and m emory by means of T-maze delayed alternation and Morris maze tasks on PD 23 and PD 70, respectively. A-1016 treatment produced only small and transien t reductions in body weight gain, and generally did not alter the thyroid s tatus of the developing rats. It did not cause any significant changes in D A or NE level, or turnover rate in any of the brain regions examined, nor d id it affect behavioral measures of cognitive development. In contrast, per inatal exposure to A-1254 led to marked deficits of growth, and sharply red uced serum T-4, although T-3 remained largely unaffected. Accompanying this hormonal imbalance, brain NE contents in the A-1254-exposed pups were redu ced, although brain DA was not significantly affected; no demonstrable neur obehavioral deficits were seen in the T-maze or Morris maze tests. These re sults indicated that development of central noradrenergic neurons was compr omised by perinatal exposure to A-1254 but not A-1016, and both PCB mixture s failed to alter behavioral performances. (C) 2001 Elsevier Science Inc.