New Treatment Strategies of Depression: Based on Mechanisms Related to Neuroplasticity

Neural Plast. 2017:2017:4605971. doi: 10.1155/2017/4605971. Epub 2017 Apr 11.

Abstract

Major depressive disorder is a severe and complex mental disorder. Impaired neurotransmission and disrupted signalling pathways may influence neuroplasticity, which is involved in the brain dysfunction in depression. Traditional neurobiological theories of depression, such as monoamine hypothesis, cannot fully explain the whole picture of depressive disorders. In this review, we discussed new treatment directions of depression, including modulation of glutamatergic system and noninvasive brain stimulation. Dysfunction of glutamatergic neurotransmission plays an important role in the pathophysiology of depression. Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, has rapid and lasting antidepressive effects in previous studies. In addition to ketamine, other glutamatergic modulators, such as sarcosine, also show potential antidepressant effect in animal models or clinical trials. Noninvasive brain stimulation is another new treatment strategy beyond pharmacotherapy. Growing evidence has demonstrated that superficial brain stimulations, such as transcranial magnetic stimulation, transcranial direct current stimulation, cranial electrotherapy stimulation, and magnetic seizure therapy, can improve depressive symptoms. The antidepressive effect of these brain stimulations may be through modulating neuroplasticity. In conclusion, drugs that modulate neurotransmission via NMDA receptor and noninvasive brain stimulation may provide new directions of treatment for depression. Furthermore, exploring the underlying mechanisms will help in developing novel therapies for depression in the future.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antidepressive Agents / therapeutic use*
  • Brain / metabolism*
  • Brain / physiopathology
  • Clinical Trials as Topic
  • Disease Models, Animal
  • Drug Partial Agonism
  • Electroconvulsive Therapy
  • Humans
  • Ketamine / administration & dosage
  • Major Depressive Disorder / metabolism*
  • Major Depressive Disorder / physiopathology
  • Major Depressive Disorder / therapy*
  • Neuronal Plasticity*
  • Receptors, Metabotropic Glutamate / antagonists & inhibitors
  • Receptors, N-Methyl-D-Aspartate / agonists
  • Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Signal Transduction
  • Synaptic Transmission
  • Transcranial Direct Current Stimulation
  • Transcranial Magnetic Stimulation
  • Treatment Outcome

Substances

  • Antidepressive Agents
  • NR2B NMDA receptor
  • Receptors, Metabotropic Glutamate
  • Receptors, N-Methyl-D-Aspartate
  • Ketamine