• Ying Cheng, Adia Thomas, Feras Mardini, Shannon L Bianchi, Junxia X Tang, Jun Peng, Huafeng Wei, Maryellen F Eckenhoff, Roderic G Eckenhoff, and Richard J Levy.
• Division of Anesthesiology and Pain Medicine, Children's National Medical Center, The George Washington University School of Medicine and Health Sciences, Washington, DC, United States of America.
• Plos One. 2012 Jan 1; 7 (2): e32029.

AbstractCarbon 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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