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Deep-brain subthalamic nucleus stimulation (DBS-STN) has become a well-established therapeutic option for advanced Parkinson's disease (PD). While the motor benefits of DBS-STN are widely acknowledged, the neuropsychiatric effects are still being investigated. Beyond its immediate effects on neuronal circuits, emerging research suggests that DBS-STN might also modulate the peripheral inflammation and neuroinflammation. In this work, we assessed the effects of DBS-STN on food-related motivation, food intake pattern, and the level of anxiety and compared them with markers of cellular and immune activation in nigrostriatal and mesolimbic areas in rats with the 6-OHDA model of early PD. To evaluate the potential mechanism of observed effects, we also measured corticosterone concentration in plasma and leukocyte distribution in peripheral blood. We found that DBS-STN applied during neurodegeneration has beneficial effects on food intake pattern and motivation and reduces anxiety. These behavioral effects occur with reduced percentages of IL-6-labeled cells in the ventral tegmental area and substantia nigra pars compacta in the stimulated brain hemisphere. At the same brain structures, the cFos cell activations were confirmed. Simultaneously, the corticosterone plasma concentration was elevated, and the peripheral blood lymphocytes were reduced after DBS-STN. We believe that comprehending the relationship between the effects of DBS-STN on inflammation and its therapeutic results is essential for optimizing DBS therapy in PD. [ABSTRACT FROM AUTHOR]

Cytokines, including interleukin-10 (IL-10), are cell signaling molecules taking part in cell to cell communication, cell proliferation, differentiation, migration and apoptosis. Cytokines also have the ability to induce, regulate, and inhibit inflammation. Cytokines are produced mainly by activated peripheral immune cells, but due to dissemination of the concept of the central nervous system as an immunologically specialized zone, it is considered that cytokine signaling is one of the compo¬nents of the immune system which can modulate brain functioning. IL-10 shows immunosuppressi¬ve properties, and since expression of this cytokine has been shown in the central nervous system, researchers have started to investigate the therapeutic possibilities of IL-10 action in the context of neurodegenerative diseases, which may involve neuroinflammation in their pathogenesis. Re¬cent studies using cell cultures or animal models of neurodegenerative disorders have shown that the importance of IL-10 in the central nervous system goes beyond the anti-inflammatory activity of this cytokine. Involvement of IL-10 in neuroprotection, neurogenesis, regulation of the stress response and hippocampal synaptic plasticity connected with learning and memory is suggested. [ABSTRACT FROM AUTHOR]

Our previous study indicated that unilateral lesion of the ventral tegmental area (VTA) facilitates contralateral VTA stimulation-induced feeding or exploration. The present study was aimed to determine the possible role of the central cholinergic systems in this effect. Immunohistochemistry for choline acetyltransferase (ChAT) was used to measure the number of active cholinergic neurons in their major groups (Ch1-Ch6) and in striatal regions in rats subjected to unilateral electrocoagulation and contralateral VTA electrical stimulation (L/S group) in comparison to the unilaterally stimulated (S), unilaterally lesioned (L) and sham (Sh) groups. The study showed that unilateral VTA lesion increased (as compared to Sh group) the number of ChAT+ neurons in the Ch1-Ch3 and unilateral VTA stimulation increased the number in the Ch1 and the ventral pallidum only. The most sensitive to these changes in the mesolimbic system were cholinergic structures providing hippocampal afferentation. Surprisingly, there was no significant increase in the number of ChAT+ neurons in the L/S group. The obtained results did not confirm any evident influence of the cholinergic systems on the VTA lesion-induced facilitation of the behavioral response evoked by contralateral VTA stimulation.