The effect of social learning on a conditioned avoidance response of rats treated prenatally with aluminum lactate.

Aluminum (Al) has been proven to be a behavioral teratogenic agent in a number of experimental studies. Prenatal exposures to Al lactate have been shown to cause cognitive deficits in a variety of species. The present experiment was carried out on SPRD rat pups treated prenatally with Al lactate to determine whether observational conditioning (social learning) would reverse the impairment in learning described previously following such treatment. A conditioned avoidance response was used as an observational learning task. The results provide evidence that Al-treated pups are capable of social learning (i.e., the performance of the avoidance response improved as a result that Al-treated learning); however, the response latency of the avoidance response was not different in these animals from those that were not exposed to such facilitation, suggesting that additional factors are involved in the effects of prenatal aluminum intoxication on cognitive processes.

Effect of prenatal aluminium lactate exposure on conditioned taste aversion and passive avoidance task in the rat.

Pregnant SPRD rats were injected s.c. daily with 2.45, 4.9 and 9.8 mg kg-1 aluminium lactate or distilled water on gestational days 7-15. Gestational aluminium treatment had no effect either on litter size or the body weight of pups on postnatal day 1 but it decreased postnatal weight gain resulting in significantly lower body weight at weaning (postnatal day 22). It had no effect on the acquisition of a conditioned taste aversion, but in a passive avoidance task the learning ability of pups of dams given the top dose of aluminium was impaired.

Neurotoxicity induced by prenatal aluminum exposure in rats.

Aluminum has been implicated as a neurotoxic agent in a number of experimental laboratories and epidemiological studies. Dementia has been correlated to elevated aluminum levels in Alzheimer's disease and has been related to impaired motor function and to a number of cognitive deficits in both humans and animals. To determine the neurotoxicity of aluminum (Al) lactate exposure in rat pups, postnatal behavioral effects of 0, 2.5, 5, 10 mg/kg daily s.c. treatment during gestation days 7th-15th were investigated. Offspring were tested for motor coordination, stress tolerance in a swimming test, behavioral patterns in an open field, in the acquisition and extinction of an avoidance responding and in a reconditioning task. In the open field test the horizontal activity was diminished at the top dose of Al exposure. The motor coordination and the stress tolerance were not altered by prenatal Al treatment. The main sign of neurotoxicity was diminished performance and lengthened latency in an avoidance responding task in all treated groups. Our findings confirm that postnatal behavioral effects can be induced in offspring prenatally exposed to aluminum lactate.

Effects of prenatal triphenyl-tin exposure on the development of behavior and conditioned learning in rat pups.

Neurotoxic effects of the fungicide triphenyl-tin acetate were examined in pups of mothers treated perorally on day 7-15 of gestation. The gait and development of motor coordination did not differ from those of control animals, in spite of the high mortality rate of control pups during the nursing period. Spontaneous locomotor activity of treated pups at the age of 23 and 36 days was increased, however by the age of 90 days activity returned to control levels. Conditioned avoidance was acquired more rapidly, but was also extinguished sooner in animals born from, the nursed by poisoned mothers than in control.