use of antidepressants in anxiety disorders and in chronic pain states

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J Psychiatry Neurosci 2001 Jan;26(1):37-43 Related Articles, Books

Putative mechanisms of action of antidepressant drugs in affective and anxiety

disorders and pain.

Blier P, Abbott FV

Departments of Psychiatry and Neuroscience, Brain Institute, University of

Florida, PO Box 100256, Gainesville, FL 32610-0256, USA.

[Medline record in process]

An enhancement of neurotransmission of serotonin (5-HT), noradrenaline, or both,

underlies the antidepressant response associated with most agents presently

available to treat major depression. With respect to the 5-HT system,

antidepressant drugs exert immediate effects on some neuronal elements

controlling overall transmission, but it is the gradual changes in neuronal

responses to such treatments that are ultimately responsible for producing their

therapeutic benefits. In major depression, an increase in 5-HT1A transmission is

thought to be a crucial determinant of the antidepressant response, whereas an

enhancement of 5-HT2 transmission in the orbitofrontal cortex may mediate the

therapeutic effect of 5-HT reuptake inhibitors in obsessive-compulsive disorder

(OCD). The doses of medication and the durations of treatment necessary to

obtain these alterations in 5-HT transmission in various brain structures of

laboratory animals are fully consistent with the conditions in the clinic

necessary to attenuate symptoms in depression and OCD. It is also possible that

the relief of chronic pain produced by some antidepressants may be mediated, in

part, by the blockade of peripheral 5-HT2A receptors. These observations

emphasize the notion that the 5-HT system is endowed with different adaptive

properties in various parts of the body, which, in addition to the multiplicity

of 5-HT receptors, makes this chemospecific network important in many disorders.

PMID: 11212592