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.
Keywords: CB1 receptor, 2-arachidonoylglycerol, fatty acid amide hydrolase, URB597, tetrahydrocannabinol, genetics, circulation.
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