New understanding of mechanisms of action of bipolar medications

J Clin Psychiatry. 2008;69 Suppl 5:22-7.

Abstract

The classical models of mood disorder pathophysiology and mechanism of antidepressant or mood stabilizing drug action focused on neurochemical deficits and the ability of medications to correct these deficits. Recent studies suggest alterations in neuroplasticity and cellular resiliency may be more closely related to the pathogenesis and pathophysiology of the disorders, as well as the mechanism of action related to effective treatments. Patients with mood disorders have been found to exhibit evidence of neuroplastic changes, such as reductions in hippocampal and cortical volume, glial and neuronal cell density, and levels of brain-derived neurotrophic factor; chronic stress, a major precipitator of depression, has been shown to cause many of the same neuroplastic changes to occur in animal models. Understanding the molecular mechanisms regulating neuroplasticity and their relationship to the pathophysiology of depression may provide insights into how current treatments work and point to novel targets for more efficacious treatments for patients with mood disorders.

Publication types

  • Review

MeSH terms

  • Animals
  • Anticonvulsants / adverse effects
  • Anticonvulsants / therapeutic use
  • Antidepressive Agents / adverse effects
  • Antidepressive Agents / therapeutic use
  • Antimanic Agents / adverse effects
  • Antimanic Agents / therapeutic use*
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Arousal / drug effects
  • Arousal / physiology
  • Bipolar Disorder / drug therapy*
  • Bipolar Disorder / physiopathology*
  • Brain / drug effects*
  • Brain / physiopathology
  • Brain-Derived Neurotrophic Factor / metabolism
  • Depressive Disorder, Major / drug therapy
  • Depressive Disorder, Major / physiopathology
  • Disease Models, Animal
  • Humans
  • Hypothalamo-Hypophyseal System / drug effects
  • Hypothalamo-Hypophyseal System / physiopathology
  • Long-Term Potentiation / drug effects
  • Long-Term Potentiation / physiology
  • Neuronal Plasticity / drug effects*
  • Neuronal Plasticity / physiology
  • Norepinephrine / metabolism
  • Pituitary-Adrenal System / drug effects
  • Pituitary-Adrenal System / physiopathology
  • Receptors, Neurotransmitter / drug effects
  • Receptors, Neurotransmitter / physiology
  • Serotonin / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / physiology

Substances

  • Anticonvulsants
  • Antidepressive Agents
  • Antimanic Agents
  • Brain-Derived Neurotrophic Factor
  • Receptors, Neurotransmitter
  • Serotonin
  • Norepinephrine