Introduction

The word inflammation derives from Latin inflammare, meaning to set in flame, and signifies the heat and redness related to an increased blood flow and vasodilation in the affected tissue. Although vasodilation, edema, and extravasation of white blood cells are the hallmarks of inflammation, its definition has become broader and has been more loosely applied to tissue reactions to injuries. With the discovery of molecules that mediate inflammation and, in particular, the extensive number of cytokines that regulate the cellular response to inflammation, an inflammatory component is now frequently ascribed to neurodegenerative diseases that were traditionally considered as noninflammatory. This is due to the production of proinflammatory cytokines in activated microglial cells and astrocytes in such diseases. The classical hallmarks of inflammation are, however, lacking.

On the other hand, events considered as components of systemic inflammation occur also in normal brain function, e.g., increase in local blood flow related to increased brain activities, and release of certain proinflammatory cytokines, including those that may be involved in mediating sleep-wakefulness.

In this overview we will focus on recent observations on how mediators of vascular responses in inflammation outside the nervous system (e.g., histamine) and proinflammatory cytokines may affect the biological clock in the brain and be involved in the regulation of the switch between sleep and wakefulness, and hence cause disturbances in the function of this switch during diseases.

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