Neurodevelopmental consequences of sub-clinical carbon monoxide exposure in newborn mice.

Neurodevelopmental consequences of sub-clinical carbon monoxide exposure in newborn mice.
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DOI:
10.1371/journal.pone.0032029
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Levy RJ
Levy RJ
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Cheng Y;Thomas A;Mardini F;Bianchi SL;Tang JX;Peng J;Wei H;Eckenhoff MF;Eckenhoff RG;Levy RJ

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Carbon monoxide (CO) exposure at high concentrations results in overt neurotoxicity. Exposure to low CO concentrations occurs commonly yet is usually sub-clinical. Infants are uniquely vulnerable to a variety of toxins, however, the effects of postnatal sub-clinical CO exposure on the developing brain are unknown. Apoptosis occurs normally within the brain during development and is critical for synaptogenesis. Here we demonstrate that brief, postnatal sub-clinical CO exposure inhibits developmental neuroapoptosis resulting in impaired learning, memory, and social behavior. Three hour exposure to 5 ppm or 100 ppm CO impaired cytochrome c release, caspase-3 activation, and apoptosis in neocortex and hippocampus of 10 day old CD-1 mice. CO increased NeuN protein, neuronal numbers, and resulted in megalencephaly. CO-exposed mice demonstrated impaired memory and learning and reduced socialization following exposure. Thus, CO-mediated inhibition of neuroapoptosis might represent an important etiology of acquired neurocognitive impairment and behavioral disorders in children.
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