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| Research article summary (published 30 Oct 1978): |
Endogenous pain control mechanisms: review and hypothesis.
Full Abstract
The anatomy, physiology, and pharmacology of an intrinsic neural network that monitors and modulates the activity of pain-transmitting neurons is reviewed. This system can be activated by opiate administration or by electrical stimulation of discrete brainstem sites. Evidence is presented that its pain-suppressing action is mediated in part by endogenous opiatelike compounds (endorphins). This pain suppression system is organized at three levels of the neuraxis: midbrain, medulla, and spinal cord. Activation of neurons in the midbrain periaqueductal gray matter (by electrical stimulation, opiates, and possibly psychological factors) excites neurons of the rostral medulla, some of which contain serotonin. The medullary neurons, in turn, project to and specifically inhibit the firing of trigeminal and spinal pain-transmission neurons. As part of a negative feedback loop, the output of the pain transmission neurons, i.e., pain itself, is an important factor in activating the pain-suppression system. A neural model which incorporates the experimental findings is proposed, and the clinical implications of the model are discussed.
Author information
Author/s: Basbaum, A I (AI); Fields, H L (HL);
Journal and publication information
Publication Type: Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
Journal: Annals of neurology (Ann Neurol), published in UNITED STATES. (Language: eng)
Reference: 1978-Nov; vol 4 (issue 5) : pp 451-62
Dates: Created 1979/03/28; Completed 1979/03/28; Revised 2006/11/15;
PMID: 216303, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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