Endocannabinoid signaling in the etiology and treatment of major depressive illness. Curr Pharm Des 2014;20(23):3795-811
Date
11/05/2013Pubmed ID
24180398Pubmed Central ID
PMC4002665DOI
10.2174/13816128113196660735Scopus ID
2-s2.0-84916885839 (requires institutional sign-in at Scopus site) 53 CitationsAbstract
The purpose of this review is to examine human and preclinical data that are relevant to the following hypotheses. The first hypothesis is that deficient CB1R-mediated signaling results in symptoms that mimic those seen in depression. The second hypothesis is that activation of CB1R-mediated signaling results in behavioral, endocrine and other effects that are similar to those produced by currently used antidepressants. The third hypothesis is that conventional antidepressant therapies act through enhanced CB1R mediated signaling. Together the available data indicate that activators of CB1R signaling, particularly inhibitors of fatty acid amide hydrolase, should be considered for clinical trials for the treatment of depression.
Author List
Hillard CJ, Liu QSAuthors
Cecilia J. Hillard PhD Associate Dean, Center Director, Professor in the Pharmacology and Toxicology department at Medical College of WisconsinQing-song Liu PhD Professor in the Pharmacology and Toxicology department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsAntidepressive Agents
Brain
Cannabis
Depressive Disorder, Major
Disease Models, Animal
Endocannabinoids
Humans
Magnetic Resonance Imaging
Neurogenesis
Polymorphism, Genetic
Receptor, Cannabinoid, CB1
Signal Transduction
