Hypomyelination, memory impairment, and blood-brain barrier permeability in a model of sleep apnea

- Intermittent hypoxia caused ultrastructural brain damage.
- Intermittent hypoxia increased serum levels of endothelin-1.
- Intermittent hypoxia did not alter the blood-brain barrier permeability.
- Intermittent hypoxia induced working memory impairment.

We investigated the effect of intermittent hypoxia, mimicking sleep apnea, on axonal integrity, blood-brain barrier permeability, and cognitive function of mice. Forty-seven C57BL mice were exposed to intermittent or sham hypoxia, alternating 30 s of progressive hypoxia and 30 s of reoxigenation, during 8 h/day. The axonal integrity in cerebellum was evaluated by transmission electron microscopy. Short- and long-term memories were assessed by novel object recognition test. The levels of endothelin-1 were measured by ELISA. Blood-brain barrier permeability was quantified by Evans Blue dye. After 14 days, animals exposed to intermittent hypoxia showed hypomyelination in cerebellum white matter and higher serum levels of endothelin-1. The short and long-term memories in novel object recognition test was impaired in the group exposed to intermittent hypoxia as compared to controls. Blood-brain barrier permeability was similar between the groups. These results indicated that hypomyelination and impairment of short- and long-term working memories occurred in C57BL mice after 14 days of intermittent hypoxia mimicking sleep apnea.