Chronic pain in mice activates Tiam1 in pyramidal neurons in the anterior cingulate cortex, increasing the number of dendritic spines and inducing synaptic plasticity. Ketamine's antidepressant effect in chronic pain is mediated by the drug blocking Tiam1-dependent maladaptive synaptic plasticity in ACC neurons.
By inhibiting NMDA receptors, ketamine increases noise to gamma frequencies in one layer of the thalamic nucleus and one lay of the somatosensory cortex. Findings suggest psychosis may be triggered by an increase in background noise impairing thalamocortical neurons which may be caused by a malfunction in NMDA receptors affecting the balance of inhibition and excitation in the brain.
Ketamine alters neural activity in the cerebral cortex, silencing normally active neurons and activating neurons that are normally inactive. The ketamine activity-induced "switch" in brain regions associated with depression may help explain its treatment effects.
Those with treatment-resistant depression showed significant improvement in symptoms and became more receptive to positive experiences following a one-week ketamine treatment regimen.
Automated computer-based training that focuses on positive words and images helps prolong the antidepressant effects of ketamine for those with treatment-resistant depression.
Mice respond better to the antidepressant effect of ketamine when the drug is delivered by men, not women, a new study reports.
Ketamine's antidepressant effect is a result of the enhancement of Kcnq2 potassium channels in a certain subtype of glutamate-sensitive neurons.
Study demonstrates the importance of a specific type of connection between neurons and may also explain how ketamine shows promise in treating depression.