Alcoholism, clinical and experimental research · 1999
Prenatal ethanol reduces the activity of adult midbrain dopamine neurons.
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Shen R Y, Hannigan J H, Kapatos G
Аннотация
BACKGROUND: Prenatal ethanol exposure has been demonstrated to reduce dopamine (DA) neurotransmission in the forebrain area, which could be contributed by altered electrical activity in midbrain DA neurons. This hypothesis was tested in the present study.
METHODS: The effects of prenatal ethanol exposure on the spontaneous activity of DA neurons in the substantia nigra and ventral tegmental area were investigated with extracellular single-unit recording techniques in adult male rats. Pregnant rats were administered single daily doses of 0, 3, or 5 g/kg ethanol via intragastric intubation from gestation day 8 through 20. An additional control group did not receive the intubation procedure.
RESULTS: Prenatal ethanol treatment significantly reduced the number of spontaneously active DA neurons in the substantia nigra and ventral tegmental area in 3- to 5-month-old male offspring. The firing rate and firing pattern of the remaining spontaneously active DA neurons were not altered. There were no differences in the spontaneous activity of DA neurons between the nonintubated and 0 g/kg control groups, indicating possible intubation-induced stress did not influence the activity of DA neurons in adult offspring. Similar prenatal ethanol effects were also determined from older animals (14-16 months old), suggesting that the reduction in the spontaneous activity of DA neurons is a persistent phenomenon in adulthood after prenatal ethanol exposure. Furthermore, the reduction in the number of spontaneously active DA neurons was not the result of a loss in DA neurons per se, as revealed by the results of tyrosine hydroxylase immunohistochemistry. The prenatal ethanol exposure-induced reduction in DA neuronal activity may result from depolarization inactivation, because systemically administered apomorphine (20 microg) increased the spontaneous activity of DA neurons.
CONCLUSIONS: Prenatal ethanol exposure induced a long-lasting reduction in the activity of midbrain DA neurons in adult animals. The effect was not the result of cell loss but possible changes in the electrical properties of DA neurons. The decreased electrical activity in midbrain DA neurons could contribute to the prenatal ethanol exposure-induced reduction in DA content and metabolites observed in previous studies and the attention/hyperactivity problems reported in children with fetal alcohol effects/fetal alcohol syndrome.
METHODS: The effects of prenatal ethanol exposure on the spontaneous activity of DA neurons in the substantia nigra and ventral tegmental area were investigated with extracellular single-unit recording techniques in adult male rats. Pregnant rats were administered single daily doses of 0, 3, or 5 g/kg ethanol via intragastric intubation from gestation day 8 through 20. An additional control group did not receive the intubation procedure.
RESULTS: Prenatal ethanol treatment significantly reduced the number of spontaneously active DA neurons in the substantia nigra and ventral tegmental area in 3- to 5-month-old male offspring. The firing rate and firing pattern of the remaining spontaneously active DA neurons were not altered. There were no differences in the spontaneous activity of DA neurons between the nonintubated and 0 g/kg control groups, indicating possible intubation-induced stress did not influence the activity of DA neurons in adult offspring. Similar prenatal ethanol effects were also determined from older animals (14-16 months old), suggesting that the reduction in the spontaneous activity of DA neurons is a persistent phenomenon in adulthood after prenatal ethanol exposure. Furthermore, the reduction in the number of spontaneously active DA neurons was not the result of a loss in DA neurons per se, as revealed by the results of tyrosine hydroxylase immunohistochemistry. The prenatal ethanol exposure-induced reduction in DA neuronal activity may result from depolarization inactivation, because systemically administered apomorphine (20 microg) increased the spontaneous activity of DA neurons.
CONCLUSIONS: Prenatal ethanol exposure induced a long-lasting reduction in the activity of midbrain DA neurons in adult animals. The effect was not the result of cell loss but possible changes in the electrical properties of DA neurons. The decreased electrical activity in midbrain DA neurons could contribute to the prenatal ethanol exposure-induced reduction in DA content and metabolites observed in previous studies and the attention/hyperactivity problems reported in children with fetal alcohol effects/fetal alcohol syndrome.