Ketamine's rapid action as an antidepressant is a result of increasing the activity of a small number of newborn neurons, which are part of ongoing neurogenesis in the brain.
Ketamine's antidepressant effect is a result of the enhancement of Kcnq2 potassium channels in a certain subtype of glutamate-sensitive neurons.
Ketamine treatment leads to an increase in IGF-1, which, in turn, produces an antidepressant effect.
Researchers report ketamine may have a broader use for the treatment of psychological disorders beyond a treatment for depression and anxiety.
Study demonstrates the importance of a specific type of connection between neurons and may also explain how ketamine shows promise in treating depression.
Combining psychological therapy with ketamine treatments resulted in longer periods of abstinence for those with severe alcohol use disorder, a new study reports.
Ketamine reduces symptoms of depression and suicidal thoughts within four hours of a single treatment, and the effects last for up to two weeks. Additional treatments may prolong the effects, researchers say.
Ketamine's rapid antidepressant action is due to specific synaptic effects, researchers report.
A new statistical model lays groundwork for understanding how ketamine induces an anesthetic response, steps to monitor unconscious patients, and provides new information about brain activity while unconscious.
In the absence of neural activity, BDNF expression can still be activated. The findings shed light on how therapeutic ketamine used has an antidepressant effect and how it works in both the long and short term.
A new study provides novel mechanistic insights into how ketamine exerts its antidepressant effects for those with depression.
The MeCP2 gene influences ketamine's behavioral effect and strengthens synapses, leading to an improvement in the drug's antidepressant effect over time.
