• Diogo Dominguini, Amanda V Steckert, Monique Michels, Mariana B Spies, Cristiane Ritter, Tatiana Barichello, Jonathan Thompson, and Felipe Dal-Pizzol.
• Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina (UNESC), Criciúma, SC, Brazil.
• Neurosci Biobehav Rev. 2021 Aug 1; 127: 504-513.

AbstractMicroglia are involved in many dynamic processes in the central nervous system (CNS) including the development of inflammatory processes and neuromodulation. Several sedative, analgesic or anaesthetic drugs, such as opioids, ∝2-adrenergic agonists, ketamine, benzodiazepines and propofol can cause both neuroprotective and harmful effects on the brain. The purpose of this review is to present the main findings on the use of these drugs and the mechanisms involved in microglial activation. Alpha 2-adrenergic agonists, propofol and benzodiazepines have several pro- or anti-inflammatory effects on microglia. Long-term use of benzodiazepines and propofol causes neuroapoptotic effects and α2-adrenergic agonists may attenuate these effects. Conversely, morphine and fentanyl may have proinflammatory effects, causing behavioural changes in patients and changes in cell viability in vitro. Conversely, chronic administration of morphine induces CCL5 chemokine expression in microglial cells that promotes their survival.Copyright © 2021. Published by Elsevier Ltd.

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