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Early studies showed that long-term encoding and retrieval of new information is associated with modulation of the theta rhythm. More recently, changes in theta power amplitude over frontal electrode sites were reported during working memory, yet their relative significance in regard to attentional and memory processes remains unclear. Event-related synchronisation responses in the 4-7.5 Hz theta EEG frequency band was studied in 12 normal subjects performing four different tasks: two working memory tasks in which load varied from one (1-back task) to two (2-back task) items, an oddball detection (attention) task and a passive fixation task. A phasic theta increase was observed following stimulus apparition on all electrode sites within each task, with longer culmination peak and maximal amplitude over frontal electrodes. Frontal theta event-related synchronization (ERS) was of higher amplitude in the 1-back, 2-back and detection tasks as compared to the passive fixation task. Additionally, the detection task elicited a larger frontal and central theta ERS than the 2-back task. By analyzing theta ERS characteristics in various experimental conditions, the present study reveals that early phasic theta response over frontal regions primarily reflects the activation of neural networks involved in allocation of attention related to target stimuli rather than working memory processes.

The 18 kDa translocator protein (TSPO) is a highly conserved protein located in the outer mitochondrial membrane. TSPO binding, as measured with positron emission tomography (PET), is considered an in vivo marker of neuroinflammation. Indeed, TSPO expression is altered in neurodegenerative, neuroinflammatory, and neuropsychiatric diseases. In PET studies, the TSPO signal is often viewed as a marker of microglial cell activity. However, there is little evidence in support of a microglia-specific TSPO expression. This review describes the cellular sources and functions of TSPO in animal models of disease and human studies, in health, and in central nervous system diseases. A discussion of methods of analysis and of quantification of TSPO is also presented. Overall, it appears that the alterations of TSPO binding, their cellular underpinnings, and the functional significance of such alterations depend on many factors, notably the pathology or the animal model under study, the disease stage, and the involved brain regions. Thus, further studies are needed to fully determine how changes in TSPO binding occur at the cellular level with the ultimate goal of revealing potential therapeutic pathways.

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