SSRI's, ketamine, and tricyclic antidepressants all bind with TrkB. The findings challenge the roles serotonin and glutamate receptors play in the effects of antidepressant medications.
A series of ketamine infusions reduced PTSD symptoms by up to 30% from baseline compared to treatment with midazolam, which reduced symptoms by 20% over the same period. Ketamine treatment significantly reduced three of four PTSD associated symptoms, including intrusive thoughts, avoidance, and negative alterations in cognition and mood.
With the risk of potential for abuse, some new fast-acting antidepressants, like Ketamine, may not be a magic "cure-all" for depression.
4E-BPs proteins are key to unlocking ketamine's antidepressant effects. When 4E-BPs are absent in neurons, ketamine can not produce its antidepressant effect.
Overactivity in the subgenual anterior cingulate cortex underlies several key symptoms of depression, anxiety, and heart disease.
Summary: An artificial neural network has identified a potential mechanism for the impaired decision-making often seen in schizophrenia patients, which involves the reduced activity of NMDA receptors.
Researchers have identified a key neural circuit that plays a role in dissociation, a phenomenon in which people can feel disconnected from their bodies and reality.
Higher doses of ketamine administered to sheep completely reduced brain activity for a short period. Researchers report as the drug wore off and consciousness was regained, the animals' brain activity switched between high and low-frequency oscillations. The timing of the brain activity corresponds to the time human users report experiencing feelings that their brain 'disconnected' from their bodies after ketamine use.
NMDA receptor hypofunction is involved in the reduction of sleep spindles and delta oscillations, which appear in the brain during deep natural sleep. Findings confirm the role NMDA receptors play in sleep disorders that accompany psychotic states.
Ketamine increases the number of serotonin 1B receptors. Ketamine binds to serotonin 1B receptors, reducing the release of serotonin and increasing the release of dopamine.
Brain connections strengthened with treatment from fast-acting antidepressants, such as ketamine, are consolidated during deep sleep. Researchers propose rapid antidepressant treatments share the ability to regulate both synaptic potentiation and homeostatic mechanisms, which may contribute to how the brain reorganizes its activity to defeat depression.
Using optogenetics to inhibit the JNK protein prevented synapses from shrinking in response to stress.
