Prenatal ethanol exposure leads to a persistent reduction in the number of spontaneously active dopaminergic (DA) neurons (DA neuron population activity) in the ventral tegmental area (VTA) in developing and adult animals. This effect might contribute to the dysfunction of the mesolimbic/cortical DA system and attention problems in children with fetal alcohol spectrum disorders. To characterize the underlying cellular mechanism for prenatal ethanol exposure-induced reduction in VTA DA neuron population activity, we used the whole-cell patch-clamp technique to study the membrane properties of putative VTA DA neurons in brain slices in 2-to 3-week-old control and prenatal ethanol-exposed animals. The results show that prenatal ethanol exposure did not impair the spontaneous pacemaker activity in putative VTA DA neurons but reduced the frequency of evoked action potentials. In addition, prenatal ethanol exposure led to a reduction in hyperpolarization-induced cation current (I h ) and an up-regulation of somatodendritic DA autoreceptors. The above prenatal ethanol exposureinduced changes could decrease the excitability of VTA DA neurons. However, they do not seem to play a role in reduced VTA DA neuron population activity in vivo, an effect thought to be mediated by excessive excitation leading to depolarization inactivation. Taken together, the above results indicate that prenatal ethanol exposure-induced reduction in VTA DA neuron population activity in vivo is not caused by changes in the intrinsic pacemaker activity or other membrane properties and could instead be caused by altered inputs to VTA DA neurons.Attention problems observed in children are among the most prominent behavioral abnormalities of fetal alcohol spectrum disorders (FASDs) (Nanson and Hiscock, 1990;Streissguth et al., 1994). Results from both human and animal studies have suggested that dysfunctions of the mesolimbic/cortical dopaminergic (DA) system, which originates in the ventral tegmental area (VTA) may contribute to attention deficit/hyperactivity disorder (Denney, 2001;Greenhill et al., 2002;Davids et al., 2003). Impaired attention (Hausknecht et al., 2005) and dysfunctions of the mesolimbic/ cortical DA system are also observed in rats with prenatal ethanol exposure. Therefore, prenatal ethanol-exposed rats are a feasible animal model to study the neural mechanism of attention problems in individuals with FASDs.The prenatal ethanol exposure-induced dysfunctions in the mesolimbic/cortical DA system include reduced DA synthesis, uptake sites, receptor binding sites, and DA metabolites in both DA neuron cell body and terminal areas (Rathbun and Druse, 1985;Cooper and Rudeen, 1988;Druse et al., 1990;Szot et al., 1999). Dopaminergic neurons also have smaller cell bodies and retarded dendritic growth in prenatal ethanol-exposed animals (Shetty et al., 1993). In addition, the sensitivity of both pre-and postsynaptic DA receptors and DA receptor-mediated behaviors are affected by prenatal ethanol exposure (Shen et al., 1995;Hannigan, ...