Examination of cortically projecting cholinergic neurons following exercise and environmental intervention in a rodent model of fetal alcohol spectrum disorders.
Examination of cortically projecting cholinergic neurons following exercise and environmental intervention in a rodent model of fetal alcohol spectrum disorders.
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DOI：
10.1002/bdr2.1839
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发表时间：
2021-02-01
影响因子：
2.1
通讯作者：
Klintsova AY
中科院分区：
文献类型：
--
作者：
Milbocker KA;Klintsova AY
在美国，多达五分之一的婴儿在出生前接触过酒精，导致被归类为胎儿酒精谱系障碍（FASD）的神经发育缺陷。补充胆碱可改善某些缺陷，提示酒精暴露（AE）扰乱胆碱能神经传递和发育。上调胆碱能神经传递的行为干预，可挽救FASD啮齿动物模型的认知缺陷。在FASD啮齿动物模型中，我们研究了两种干预(轮式跑步（WR）或“超级干预”（WR +暴露于复杂环境）对Meynert基底核（NBM）、皮质胆碱能输入源和前额叶皮层（PFC）胆碱能神经元形态的影响。总共47只雄性幼崽中有三分之一在出生后4-9天（PD）期间接受了乙醇牛奶替代品的胃内插管。另外三分之一作为假插管的程序控制，而最后三分之一作为哺乳控制。在PD 30-72期间，每组大鼠接受任意一种干预。采用胆碱乙酰转移酶（Choline acetyltransferase, ChAT+）和乙酰胆碱酯酶染色定量测定胆碱能神经元数量、体体积和轴突数量。我们的数据表明，产后治疗对成年期NBM的ChAT+神经元数量有主要影响。事后分析表明，与哺乳对照组相比，AE中ChAT+神经元数量减少（p < 0.01）。我们研究了在出生后早期AE和两次干预后，成年期NBM和PFC中胆碱能神经元的细胞结构。我们发现，AE减少了NBM中ChAT+神经元的数量，这并没有通过任何干预来缓解。
Up to 1 in 5 infants in the United States are exposed to alcohol prenatally, resulting in neurodevelopmental deficits categorized as fetal alcohol spectrum disorders (FASD). Choline supplementation ameliorates some deficits, suggesting that alcohol exposure (AE) perturbs cholinergic neurotransmission and development. Behavioral interventions, which upregulate cholinergic neurotransmission, rescue cognitive deficits in rodent models of FASD. We investigated the impacts of two interventions (either wheel-running (WR) or “super intervention,” WR plus exposure to a complex environment) on cholinergic neuronal morphology in the nucleus basalis of Meynert (NBM), the source of cortical cholinergic input, and prefrontal cortex (PFC) in a rodent model of FASD. One third of the total 47 male pups received intragastric intubation of ethanol in milk substitute during postnatal days (PD) 4–9. Another third served as sham-intubated procedural controls while the final third served as suckle controls. Rats from each group were exposed to either intervention during PD 30–72. Choline acetyltransferase (ChAT+) and acetylcholinesterase staining were used to quantify cholinergic neuron number, soma volume, and axon number. Our data indicate a main effect of postnatal treatment on ChAT+ neuron number in NBM in adulthood. Post hoc analysis demonstrates that ChAT+ neuron number is reduced in AE compared to suckle control rodents (p < .01). We examined the cytoarchitectonics of cholinergic neurons in NBM and PFC in adulthood following early postnatal AE and two interventions. We show that AE reduces ChAT+ neuron number in NBM, and this is not mitigated by either intervention.
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影响因子：
3.3
作者：
ECKENSTEIN, FP;BAUGHMAN, RW;QUINN, J
通讯作者：
QUINN, J
影响因子：
2.9
作者：
ASTLEY, SJ;WEINBERGER, E;CLARREN, SK
通讯作者：
CLARREN, SK
影响因子：
2.5
作者：
DOBBING, J;SANDS, J
通讯作者：
SANDS, J
影响因子：
2.5
作者：
CANDY, JM;PERRY, EK;EDWARDSON, JA
通讯作者：
EDWARDSON, JA
影响因子：
2.9
作者：
DRISCOLL, CD;STREISSGUTH, AP;RILEY, EP
通讯作者：
RILEY, EP