Postnatal Ethanol Exposure Simplifies the Dendritic Morphology of Medium Spiny Neurons Independently of Adenylyl Cyclase 1 and 8 Activity in Mice

Abstract

These data indicate that neonatal exposure to a single dose of EtOH is sufficient to cause long-term alterations in the dendritic complexity of MSNs and that this outcome is not altered by the functional status of AC1 and AC8. Therefore, although deletion of AC1/8 demonstrates a role for the ACs in normal morphologic development and EtOH-induced neurodegeneration, loss of AC1/8 activity does not exacerbate the effects of EtOH on dendritic morphology or spine density.