Postnatal ethanol exposure simplifies the dendritic morphology of medium spiny neurons independently of adenylyl cyclase 1 and 8 activity in mice.
Postnatal ethanol exposure simplifies the dendritic morphology of medium spiny neurons independently of adenylyl cyclase 1 and 8 activity in mice.
复制标题
出生后乙醇暴露简化了小鼠中型多棘神经元的树突形态，与腺苷酸环化酶 1 和 8 活性无关。
DOI：
10.1111/acer.12383
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Conti,AlanaC
中科院分区：
文献类型：
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作者：
Susick,LauraL;Lowing,JenniferL;Provenzano,AnthonyM;Hildebrandt,ClaraC;Conti,AlanaC
BackgroundFetal exposure to alcohol can have multiple deleterious effects, including learning disorders and behavioral and executive functioning abnormalities, collectively termed fetal alcohol spectrum disorders. Neonatal mice lacking both calcium‐/calmodulin‐stimulated adenylyl cyclases (ACs) 1 and 8 demonstrate increased vulnerability to ethanol (EtOH)‐induced neurotoxicity in the striatum compared with wild‐type (WT) controls. However, the developmental impact on surviving neurons is still unclear.MethodsWT and AC1/8 double knockout (DKO) mice were administered 1 dose of EtOH (2.5 g/kg) between postnatal days 5 to 7 (P5–7). At P30, brains were removed and processed for Golgi–Cox staining. Medium spiny neurons (MSNs) from the caudate putamen were analyzed for changes in dendritic complexity; number of branches, branch points and terminals, total and average dendritic length; spine density and soma size.ResultsEtOH significantly reduced the dendritic complexity and soma size in surviving MSNs regardless of genotype without affecting spine density. In the absence of EtOH, genetic deletion of AC1/8 reduced the dendritic complexity, number of branch points, spine density, and soma size of MSNs compared with WT controls.ConclusionsThese 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.
