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Recent work has demonstrated an age-dependent ketogenic neuroprotection after traumatic brain injury (TBI), where younger post-weaned animals maintained on the ketogenic (KG) diet showed reduction in cortical contusion volumes and preservation of cortical neurons when compared with animals on a standard diet. It was hypothesized that maturational differences in cerebral transport of ketones via the monocarboxylate transporter (MCT2) account for this agedependent ketogenic neuroprotection. PND35 (N ϭ 24) and 75 (n ϭ 23) rats were immediately placed on either a standard or KG diet following sham surgery or controlled cortical impact injury. Animals were perfused with 4% paraformaldehyde at 1 hr, 6 hrs, 24 hrs, 3 days, or 7 days after injury and the brain sections (50m) were processed for MCT2 immunohistochemistry. A separate group of animals were processed for MCT2 western blot analysis. PND35 and 75 animals showed increased MCT2 immunoreactivity in the cerebral vasculature. While the western blot analysis of the ipsilateral cortices confirmed a gradual increase in MCT2 expression among both age groups post-injury, MCT2 expression increases earlier in the younger brain (1 hr) and achieves a 1.7-fold greater increase by 24 hrs compared to the adult brain. The finding that there is up-regulation of MCT2 after TBI and that this up-regulation occurs rapidly are both novel results. The previously observed agedependent ketogenic neuroprotection is likely related to agerelated differences in the "inducibility" of the ketone transporter and suggests that alternative substrate therapy has potential applications for younger head-injured patients. NS30308, NS37365, NS27544, NS02197 and the Lind Lawrence Foundation.
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