Antidepressant drug action — From rapid changes on network function to network rewiring

摘要: Abstract There has been significant recent progress in understanding the neurobiological mechanisms of antidepressant treatments. The delayed-onset action monoamine-based drugs have associated to their ability slowly increase synaptic plasticity and neuronal excitability via altering neurotrophic signaling (synthesis BDNF activation its receptor TrkB), dematuration GABAergic interneurons inhibition “breaks plasticity”. On other hand, antidepressants rapidly regulate emotional processing that – with help heightened appropriate rehabilitation gradually lead changes on functional connectivity clinical recovery. Moreover, discovery rapid-acting antidepressants, most notably ketamine, inspired interest for novel developments better efficacy faster onset action. Therapeutic effects linked thereby translation release BDNF, TrkB–mTOR–p70S6k pathway increased synaptogenesis within prefrontal cortex. Thus, alterations TrkB signaling, are shared phenomena implicated responses produced by both rapid acting antidepressants. However, regardless antidepressant, therapeutic not permanent which suggests network function remain unstable vulnerable psychosocial challenges.