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Expression and Localization of the Orexin-1 Receptor (OX1R) After Traumatic Brain Injury in Mice

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Abstract

Orexins are neuropeptides that have a wide range of physiological effects, and recent studies have suggested that the orexin system may be involved in traumatic brain injury. However, the expression and localization of orexin receptors have not been examined yet under brain injury conditions. In the present study, we used immunohistochemical techniques to investigate the expression of orexin-1 receptor (OX1R) and its time-dependent changes in the mouse brain after controlled cortical impact (CCI) injury. OX1R-like immunoreactivity was first detected 6 h after injury in the surrounding penumbra of the injury. The intensity of this immunoreactivity was increased at 12 h, peaked at day 1, and then decreased from day 2 to day 7. To identify the cellular localization of OX1R, we also performed double-immunohistochemical staining with OX1R and several cell marker antibodies. OX1R-like immunopositive cells were clearly co-localized with immunoreactivity for the neuronal marker NeuN at day 7. It was also expressed on the periphery of cells immunopositive for CD11b, a microglial cell marker, at days 1 and 7. These results suggest that orexin and its receptor may play roles in traumatic brain injury, and that OX1R is induced in neurons and microglial cells after traumatic brain injury.

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Acknowledgments

This study was supported in part by grants from the Ministry of Education, Science, Sports and Culture, from a Showa University Grant-in Aid for Innovative Collaborative Research Projects, and from a Special Research Grant-in Aid for Development of Characteristic Education from the Japanese Ministry of Education, Culture, Sports, Science and Technology.

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Correspondence to Seiji Shioda.

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Mihara, Y., Dohi, K., Yofu, S. et al. Expression and Localization of the Orexin-1 Receptor (OX1R) After Traumatic Brain Injury in Mice. J Mol Neurosci 43, 162–168 (2011). https://doi.org/10.1007/s12031-010-9438-6

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  • DOI: https://doi.org/10.1007/s12031-010-9438-6

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