Repetitive acute intermittent hypoxia does not promote generalized inflammatory gene expression in the rat CNS

• rAIH (ten, 5-min hypoxic episodes, thrice weekly, 4 weeks) promotes neuroplasticity.
• rAIH at this time does not promote generalized neuroinflammation.
• rAIH also does not appear to promote generalized systemic inflammation.
• Unlike CIH, rAIH may be a safer option to enhance motor neuron function.
• Additional studies with longer term rAIH treatments remain necessary.

Modest protocols of repetitive acute intermittent hypoxia (rAIH) enhance motor function in patients with chronic incomplete spinal injury. Since chronic intermittent hypoxia (CIH) elicits neuroinflammation, there is potential for rAIH to have similar effects. Thus, we tested the hypothesis that rAIH has minimal impact on microglial inflammatory gene expression, but up-regulates key neurotrophic factor expression in a CNS region-specific manner. Using real time PCR, we evaluated mRNA levels of inflammatory and neurotrophic factors in immunomagnetically-isolated microglia from rat frontal cortex, brainstem and upper and lower cervical spinal cord following rAIH (ten, 5-min episodes, thrice weekly, 4 weeks). In agreement with our hypothesis, rAIH had no significant impact on microglial inflammatory gene expression in any region studied. On the other hand, neurotrophic factor expression was altered in a gene- and region-specific pattern. These results have important implications for the safety of rAIH as a potential therapy to enhance neuroplasticity and motor function in patients with spinal injury or other neurologic disorders.