Ketamine, a sedative and dissociative anesthetic developed in the 1960s as an alternative to phencyclidine (PCP), has been used clinically for over 50 years. It causes fewer severe side effects like hallucinations than PCP, leading to its popularity in emergency medicine and surgeries requiring rapid induction and recovery. Over recent decades, ketamine has been found effective for additional conditions, including acute and chronic pain management and psychiatric disorders such as major depression. It is also a common drug of abuse sought for its hallucinogenic and sedative effects. This review explores ketamine's clinical and non-clinical uses and its impact on patient care.
Chronic pain activates specific MKP/DUSP genes in limbic brain regions, which may contribute to the development of depression. Male rats exposed to 21 days of inflammatory pain showed increased MKP-1 expression in the hippocampus, prefrontal cortex, and anterior cingulate cortex. Female rats also showed increased hippocampal MKP-1, but MKP-1 decreased in the anterior cingulate cortex and did not change in the prefrontal cortex. Similar region-specific changes occurred for MKP-2 and MKP-3. Low-dose ketamine (10 mg/kg) blocked pain-induced upregulation of limbic MKP-1. The findings suggest dysregulation of these genes may underlie mood disorders associated with chronic pain.