Abstract
Tramadol is an analgesic that is used worldwide, but its mechanisms of action have not been elucidated. It has been speculated that tramadol acts primarily through the activation of µ-opioid receptors and the inhibition of monoamine reuptake. The majority of studies to date have focused on ion channels in the central nervous system as targets of anesthetics and analgesics. During the past decade, major advances have been made in our understanding of the physiology and pharmacology of G-protein coupled receptor (GPCR) signaling. Several studies have shown that GPCRs and ion channels are targets for analgesics and anesthetics. In particular, tramadol has been shown to affect GPCRs, including muscarinic acetylcholine receptors and 5-hydroxytryptamine receptors. Here, the effects of tramadol on monoamine transporters, GPCRs, and ion channels are presented, and recent research on the pharmacology of tramadol is discussed.
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