Abstract
The need for understanding the mechanisms of ketamine action in the brain has pushed research to measure the effect of ketamine on neurotransmitters. In fact, ketamine binds to a variety of receptors, but principally acts at the N-methyl-D-aspartate receptor (NMDAR) thus being responsible for NMDAR blockade and/or hypofunction. This hypofunction can explain connectional and oscillatory abnormalities considered as a consequence of a weakened excitation of inhibitory gamma-aminobutyric acidergic interneurons that synchronize cortical networks and disinhibition of principal cells. The chapter reviews the studies that have investigated about the changes on the neurotransmitter pools until now to provide robust evidences of the most recent theory of the action of ketamine on human and animal brain.
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