ABSTRACT
Carbon monoxide (CO) poisoning has been a well-known cause of a wide variety of neurologic and psychiatric problems. This chapter summarizes some of data on CO-induced impairment of learning, memory, and neuronal dysfunction in mice and rats. Neuronal damage induced by successive CO exposures was more extensive and severe than that by single CO exposure. K. Kaltwasser et al. reported that CO toxicity was reduced in rats with chlorpro-mazine-induced hypothermia. It has also been reported that post-ischemic hypothermia acts protectively against ischemic brain damage in the rat and gerbil. Delayed neuronal damage and deficiencies in learning and memory were also produced after CO exposure in mice. This memory deficiency also develops in a delayed manner, more than 3 d after CO exposure. CO readily combines with hemoglobin to form carboxyhemoglobin, preventing the transfer of oxygen to tissues. Tissues such as the brain depend mainly on aerobic metabolism, so a deficiency of oxygen supply damages normal cell functions.
