Changes in inflammatory cascades have been implicated in the underlying pathophysiology of psychosis. Translocator protein 18 kDa (TSPO) has been used to assess neuroinflammatory processes in psychotic disorders. Nonetheless, it is unclear whether TSPO, a mitochondrial protein, can be interpreted as a general marker for inflammation in diseases involving psychosis. To address this question, we investigated TSPO signaling in representative mouse models for psychosis with inflammatory disturbances. The maternal immune activation and cuprizone short-term exposure models show different TSPO signaling. Furthermore, we observed similarities and differences in their respective stress pathways including stress hormone signaling and oxidative stress that are functionally interconnected with the inflammatory responses. We propose that more careful studies of TSPO distribution in neuroinflammation and other stress cascades associated with psychotic symptoms will allow us to understand the biological mechanisms underlying psychosis-related behaviors.
Keywords: Cuprizone short-term exposure (CSE); Inflammatory disturbances; Maternal immune activation (MIA); Psychosis; Stress cascades; Translocator protein 18 kDa (TSPO).
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