By blocking glutamate from binding to the NMDA receptor, ketamine leads to an augmented glutamate release, which activates other types of glutamate receptors and enhances the function and density of synapses (the junctions between neurons) in areas of the brain where stress or depression has caused cells to atrophy. Increased synaptic plasticity – the ability of synapses to adjust their strength, which is essential to healthy brain function – could be the neurobiological reason for the apparent therapeutic effect in patients.