Prenatal
ethanol exposure has been shown to produce a persistent reduction in the spontaneous activity of ventral tegmental area (VTA)
dopamine (DA) neurons and in DA neurotransmission.
Amphetamine-like stimulants are effective in treating
attention deficit/hyperactivity disorder (
ADHD), which is a major symptom in
fetal alcohol syndrome. Because there is a link between reduced DA neurotransmission and
ADHD, we investigated the possibility that
amphetamine could restore the spontaneous activity of VTA DA neurons. Pregnant rats were administered 0 or 6 g/kg/day
ethanol via intragastric intubation during gestation days 8 to 20. The spontaneous activity of VTA neurons was studied in 6- to 8-week-old male offspring using extracellular single-unit recording in unanesthetized (paralyzed, locally anesthetized) or
chloral hydrate-anesthetized rats. Prenatal
ethanol exposure reduced the number of spontaneously active DA neurons without changing the firing rate or firing pattern in both groups of animals. Acute
amphetamine administration (2 mg/kg, i.v.) increased the number of spontaneously active DA neurons after prenatal
ethanol exposure. Because
amphetamine inhibited DA neuron firing rate in
ethanol-exposed animals, it is possible that
amphetamine restored the number of spontaneously active neurons by alleviating the depolarization block. These results show that the reduction in the number of spontaneously active DA neurons resulting from prenatal
ethanol exposure is not confounded by using
general anesthesia. Furthermore, acute
amphetamine treatment can normalize the activity of DA neurons after prenatal
ethanol exposure. This mechanism may contribute to the
therapeutic effects of
amphetamine-like stimulants in attention problems observed in children with
fetal alcohol syndrome.